Information

Mutations, Death and the theory of Evolution

Mutations, Death and the theory of Evolution


We are searching data for your request:

Forums and discussions:
Manuals and reference books:
Data from registers:
Wait the end of the search in all databases.
Upon completion, a link will appear to access the found materials.

Evolution always made sense to me and I still find it to be true. However, I quite recently found a comment online that gave me some doubts and made me curious on the subject. Although a student of biology, I don't really know genetics all that much (I'm more of an ecology type), so I'm asking here - I hope there's somebody who can help. Without further ado, how would you respond to this comment (fyi the original post was on the subject of a woman denying evolution, then talking about her new short-eared dog breed):

"The woman was probably demonstrating that changes that we see in dogs (variation within one kind) is NOT Evolution because it cannot create new genetic info (so it cannot explain the origin of organs). It causes CHANGE with what is already there, and these changes are only NEGATIVE or NEUTRAL (but often negative, that's why our dogs are degenerate from wolves). I used to make a living out of Selective Breeding so I know that you can only change a fish's color and size but you can never add feathers or wings or limbs to it since the codes for those doesn't exist in a fish, nor can we create one just by random mutation. That's like trying to create Windows10 OS by relying on random bit-rot/data corruption -- death of program is ensured. The word "engineering" in Genetic Engineering isn't there for no reason. Coding genetic programs requires more intellect than coding binaries. Literally, we're all digital programs (but very intelligently coded). Welcome to modern science.

Having said that, you do realize that the reason why you grow old is because of mutations, right? I will be neutral here (neither Evolutionist nor Creationist) but let's be realistic. If mutations can improve us, why do we grow old and die from it even though our body undergoes "selection" too? And you do know that our genome as a population is also getting older, right? Let's math this out: Let's say you're Adam with no mutations yet. Your offspring will inherit an average of 50 mutations from you (you generated this mutations as you grow old). Let's say that we die when reaching 10,000 mutations (Natural Selection). Your offspring started his life on earth a little bit older than you. And he shall add your 50 mutation, plus his own 50 mutation to his offspring. The 3rd generation will now start his life with 100 mutations. Some may mutate faster, but since ALL organism mutates and pass it down, it's easy to see where all of us will end up. Think of your last PC. :)"


Introduction

Welcome to Biology.SE. Please see my comment for issues relating the form of your question. Below my answers are very short as it would take too long to give complete answer. I just redirect you toward a source of information.

Questions

Having said that, you do realize that the reason why you grow old is because of mutations, right?

No, that's wrong!

I will be neutral here (neither Evolutionist nor Creationist) but let's be realistic. If mutations can improve us, why do we grow old and die from it even though our body undergoes "selection" too?

Nope, our body does not undergo "selection". (At least not in any way you may have meant it!)

And you do know that our genome as a population is also getting older, right?

No, that's wrong!

Let's math this out: Let's say you're Adam with no mutations yet.

There was no such thing as a first human and no perfect human free of any deleterious mutations. Adam and Eve are characters from the christian mythology (kind like the equivalent of the first unnamed man Epimetheus and Prometheus created and Pandora (first woman) that Zeus created to punish men).

Your offspring will inherit an average of 50 mutations from you (you generated this mutations as you grow old).

Good job, this is a relatively realistic number (although a bit too high) of new mutations a human baby inherits. Note that these new mutations occur in the ovaries and in the testis either during mitosis or during the meiosis (mutation rate is much higher during meiosis).

Let's say that we die when reaching 10,000 mutations (Natural Selection). Your offspring started his life on earth a little bit older than you. And he shall add your 50 mutation, plus his own 50 mutation to his offspring. The 3rd generation will now start his life with 100 mutations. Some may mutate faster, but since ALL organism mutates and pass it down, it's easy to see where all of us will end up. Think of your last PC. :)"

Most mutations are neutral. Those that are deleterious are (most often) washed out by selection and therefore do not accumulate in the way you describe.

Source of information

I cannot provide complete answers as it would unfortunately be too much for a single post. Instead I redirect you to an online source of information.

There are great (free) online courses. Consider for example having a look at Understanding Evolution (by UC Berkeley). It is a very introductory source of information on evolutionary biology. It is quite short and you will quickly learn a lot!


The new mutation theory of phenotypic evolution

Recent studies of developmental biology have shown that the genes controlling phenotypic characters expressed in the early stage of development are highly conserved and that recent evolutionary changes have occurred primarily in the characters expressed in later stages of development. Even the genes controlling the latter characters are generally conserved, but there is a large component of neutral or nearly neutral genetic variation within and between closely related species. Phenotypic evolution occurs primarily by mutation of genes that interact with one another in the developmental process. The enormous amount of phenotypic diversity among different phyla or classes of organisms is a product of accumulation of novel mutations and their conservation that have facilitated adaptation to different environments. Novel mutations may be incorporated into the genome by natural selection (elimination of preexisting genotypes) or by random processes such as genetic and genomic drift. However, once the mutations are incorporated into the genome, they may generate developmental constraints that will affect the future direction of phenotypic evolution. It appears that the driving force of phenotypic evolution is mutation, and natural selection is of secondary importance.

For the last six decades, the dominant theory of evolution has been neo-Darwinism, which was developed by the three founders of theoretical population genetics, Fisher (1), Wright (2), and Haldane (3), and was later supported by various evolutionists (4–9). Neo-Darwinism asserts that natural selection is the driving force of evolution, and mutation merely provides raw genetic materials with which natural selection produces novel characters. This view is based on the argument that natural selection enhances the frequencies of advantageous alleles at many loci and makes it easy to recombine them into a single individual and produce a novel character, especially in the presence of gene interaction (1–3). By following this principle, evolutionary biologists have developed various theories of natural selection to explain the evolution of sex (9), formation of new species (10), development of social life in insects (11), evolution of altruism (12), etc. In these studies, it is customary to assume that there is a sufficient amount of genetic variation within populations, and therefore what is necessary is to study how natural selection produces complex characters or complex ways of life.

In the last four decades, the study of molecular evolution has shown that a majority of amino acid substitutions in proteins are neutral or nearly neutral and that only a minority of the substitutions change protein function (13–18). It has also been shown that the major factor of evolution at the molecular level is mutation, including gene duplication and other genetic changes (15–17). However, most evolutionists still believe in neo-Darwinism with respect to phenotypic evolution and are not interested in neutral evolution (19–22). Mayr (23) stated that neutral mutations apparently occur at the molecular level, but because they do not affect phenotypic characters, they are of little interest to evolutionists. In this respect, it is interesting to note that even Kimura (15), protagonist of the neutral theory of molecular evolution, believed in neo-Darwinism with respect to phenotypic evolution. By contrast, Nei (17, 24, 25) argued that because phenotypic characters are ultimately controlled by DNA sequences, both molecular and phenotypic evolution must occur in similar ways. He also suggested that a considerable portion of morphological evolution is caused by neutral or nearly neutral mutations, and the driving force of evolution is mutation at both molecular and phenotypic levels. However, the evidence for supporting this argument was rather weak.

In recent years substantial progress has occurred in the study of the molecular basis of phenotypic evolution, so that we can examine the relative importance of mutation and selection in detail. In this article, I will first consider phenotypic evolution controlled by multigene families, because there is a large amount of interesting data, and the interpretation of new findings in this area is relatively simple. I will then discuss the evolutionary changes of protein-coding and regulatory regions of genes in relation to phenotypic evolution and their implications for the general theory of evolution.


Rapid evolution of the human mutation spectrum

DNA is a remarkably precise medium for copying and storing biological information. This high fidelity results from the action of hundreds of genes involved in replication, proofreading, and damage repair. Evolutionary theory suggests that in such a system, selection has limited ability to remove genetic variants that change mutation rates by small amounts or in specific sequence contexts. Consistent with this, using SNV variation as a proxy for mutational input, we report here that mutational spectra differ substantially among species, human continental groups and even some closely related populations. Close examination of one signal, an increased TCC→TTC mutation rate in Europeans, indicates a burst of mutations from about 15,000 to 2000 years ago, perhaps due to the appearance, drift, and ultimate elimination of a genetic modifier of mutation rate. Our results suggest that mutation rates can evolve markedly over short evolutionary timescales and suggest the possibility of mapping mutational modifiers.

Keywords: DNA replication and repair Human population structure evolutionary biology genomics great ape evolution human mutagenesis mutational signatures population genetics.

Conflict of interest statement

The authors declare that no competing interests exist.

Figures

Figure 1.. Global patterns of variation in…

Figure 1.. Global patterns of variation in SNV spectra.

( A ) Principal component analysis…

Figure 1—figure supplement 1.. Pairwise mutation spectrum…

Figure 1—figure supplement 1.. Pairwise mutation spectrum comparisons among continental groups.

Figure 1—figure supplement 2.. PCA of all…

Figure 1—figure supplement 2.. PCA of all 1000 Genomes continental groups.

Figure 1—figure supplement 3.. Mutation spectrum comparison…

Figure 1—figure supplement 3.. Mutation spectrum comparison p-values.

Each left-hand plot shows all chi-squared p-values…

Figure 1—figure supplement 4.. The effects of…

Figure 1—figure supplement 4.. The effects of biased gene conversion on mutation spectra.

Figure 1—figure supplement 5.. Mutation spectra of…

Figure 1—figure supplement 5.. Mutation spectra of transcribed vs non-transcribed DNA.

Figure 1—figure supplement 6.. Mutation spectra of…

Figure 1—figure supplement 6.. Mutation spectra of ChromHMM chromatin states (Part I of II).

Figure 1—figure supplement 7.. Mutation spectra of…

Figure 1—figure supplement 7.. Mutation spectra of ChromHMM chromatin states (Part II of II).

Figure 1—figure supplement 8.. Variation of the…

Figure 1—figure supplement 8.. Variation of the mutation spectrum with DNA replication timing.

Figure 2.. Concordance of mutational shifts in…

Figure 2.. Concordance of mutational shifts in 1000 Genomes versus SGDP.

Each panel shows natural-log…

Figure 2—figure supplement 1.. Heatmap comparisons between…

Figure 2—figure supplement 1.. Heatmap comparisons between continental groups in 1000 Genomes and the SGDP.

Figure 2—figure supplement 2.. Regression of the…

Figure 2—figure supplement 2.. Regression of the SGDP heatmap coefficients versus the corresponding 1000 Genomes…

Figure 3.. Geographic distribution and age of…

Figure 3.. Geographic distribution and age of the TCC mutation pulse.

Figure 3—figure supplement 1.. TCC → TTC…

Figure 3—figure supplement 1.. TCC → TTC mutation fraction as a function of allele frequency…

Figure 3—figure supplement 2.. Fraction of TCC…

Figure 3—figure supplement 2.. Fraction of TCC → TTC mutations as a function of allele…

Figure 3—figure supplement 3.. Mutation type enrichment…

Figure 3—figure supplement 3.. Mutation type enrichment as a function of allele frequency in UK10K…

Figure 3—figure supplement 4.. Mutation type enrichment…

Figure 3—figure supplement 4.. Mutation type enrichment as a function of allele frequency in UK10K…

Figure 3—figure supplement 5.. Mutation type enrichment…

Figure 3—figure supplement 5.. Mutation type enrichment as a function of allele frequency in UK10K…

Figure 3—figure supplement 6.. Mutation spectrum comparisons…

Figure 3—figure supplement 6.. Mutation spectrum comparisons partitioned by allele frequency.

Figure 4.. Mutational variation among east Asian…

Figure 4.. Mutational variation among east Asian populations.

( A ) PCA of east Asian…

Figure 4—figure supplement 1.. Mutation spectrum differences…

Figure 4—figure supplement 1.. Mutation spectrum differences within Africa, Europe, East Asia, and South Asia.


Darwin and Evolution vs. God

The debate between evolution and intelligent design continues, even if some evolutionists claim victory.

On the anniversary of the birth of naturalist Charles Darwin, Feb. 12, Phil Plait wrote, &ldquoEvolution is the basis for all modern biology. It is the central tenet, the organizing theme, the trunk from which all branches grow.&rdquo

But does evolution really define the basis for all modern biology? Does the principle of ever-better random mutation really work as it is widely advertised and accepted?

The overwhelmingly negative nature of mutations

Barney Maddox, M.D., writes, &ldquoThe underlying genetic mechanism of evolution is random mutation, and specifically mutation that is beneficial to life. Biology textbooks in theory present positive and negative mutations to students as though these were commonplace and roughly equal in number. However, these books fail to inform students that unequivocally positive mutations are unknown to genetics, since they have never been observed (or are so rare as to be irrelevant).

&ldquoThe biology textbooks in other chapters teach that most mutations are pathologic, or disease-causing, but they don&rsquot apply that information to evolution. The worst diseases doctors treat today are caused by genetic mutations. Nearly 4,000 diseases are caused by mutations in DNA.

&ldquo&lsquoThe human genome contains a complete set of instructions for the production of a human being. &hellip Genome research has already exposed errors [mutations] in these instructions that lead to heart disease, cancer, and neurological degeneration&rsquo [The Human Genome Project, announcement from the University of Texas Southwestern Medical School, May 6, 1993].

&ldquoThese diseases are crippling, often fatal, and many of the affected pre-born infants are aborted spontaneously, i.e., they are so badly damaged they can&rsquot even survive gestation. However, the biology textbooks, when discussing mutation in evolution, only discuss the very rare &lsquopositive&rsquo mutation, like sickle cell anemia. The fact of some 4,000 devastating genetic diseases is suppressed from publication&rdquo (Institute for Creation Research).

Dulled senses?

How is it that, in spite of the well-documented data championed by an ever-growing list of dissenting scientists, society at large rushes toward the blind canyon of impending demise facilitated by pure godless evolution?

Is there some diabolical unseen hand at work, orchestrating a colossal conspiracy that has dulled the senses of otherwise thoughtful and logical people?

The Holy Bible is generally unread&mdashexcept as pleasant prose&mdashby society in our post-Christian environment. It is consistently ignored as a source of reliable facts that could reveal the status of mankind in relation to the unseen spirit world&mdasha world that can&rsquot be observed by science.

Revelation 12:9 pulls back the curtain to that spirit world: &ldquoThe great dragon was cast out, that serpent of old, called the Devil and Satan, who deceives the whole world he was cast to the earth, and his angels were cast out with him.&rdquo

Similarly, Ephesians 6:12 tells us, &ldquoFor we do not wrestle against flesh and blood, but against principalities, against powers, against the rulers of the darkness of this age, against spiritual hosts of wickedness in the heavenly places.&rdquo

Evolution squarely frames one of the great conspiracies that Satan has so effectively nurtured to lead the entire human race off the course that leads to peace, safety, happiness and eternal life, and onto the wrong track that ends so abruptly in a futureless chasm of death and destruction.

What drives evolution?

What really drove the development of evolution and its acceptance? Was it the surprise discovery of a finely tuned system of random mutations resulting in the spectacular blossoming of an innumerable variety of incredibly intricate living biological systems that thrive in a virtual perpetual motion of arrival, survival and procreation? (No, since such mutations have not been discovered, only assumed.)

Or was it a desperate attempt to explain the existence of all things without the introduction of a creator?

It seems some atheists imagine and reject a bipolar god who created a gorgeous cosmos, but then abandoned His masterpiece to spiritual decay, pain and suffering.

But is that reality? Is there a benevolent extraterrestrial genius architect out there who painstakingly designed and produced the human race?

What God says

Science can&rsquot explore the spiritual realm. The only insight we could have into the nonphysical realm would have to come from a revelation from that realm.

The Bible claims to be that revelation. It shows that God has a plan of enormous scope to affectionately, lovingly reinvigorate and retrain the wayward human race, including virtually every single soul who has already lived and died, to join Him in eternal, meaningful life.

Consider a few quotes from the Bible about the future God has planned and will bring for humanity:

    : &ldquoThe kingdoms of this world have become the kingdoms of our Lord and of His Christ, and He shall reign forever and ever!&rdquo : &ldquoAnd I saw the dead, small and great, standing before God.&rdquo : &ldquoOf the increase of His government and peace there will be no end&rdquo (emphasis added).

The Creator God is not evil, and He has not abandoned His creation. He plans to end war, to offer a real chance to everyone and to set up an eternal Kingdom of peace.

Learn more about the Creator in the article &ldquoIntelligent Design: Can Science Answer the Question, Does God Exist?&rdquo Learn more about His awesome plan in the sections on &ldquoWhat Is the Meaning of Life?&rdquo and the &ldquoKingdom of God.&rdquo

Sam Shrauner

Sam Shrauner is an elder in the Lakeland, Florida, congregation of the Church of God, a Worldwide Association.


How are Mutation and Natural Selection related? Let’s Know!

1. Both Mutation and Natural Selection are the mechanisms of evolution

Evolution is the framework to understand the origination of new species. They are five mechanisms of evolution and these are mutation, genetic drift, gene flow, non-random mating, and natural selection.

Each mechanism of evolution can be characterized by how it affects fitness, adaptation, the average phenotype of a trait in a population, and the genetic diversity of the population.

Mechanism of evolution is the working of the evolution process that helps us better understand how, when, and why the organisms have evolved.

Both mutation and natural selection are the working mechanisms of evolution. Mutation causes genotypic variations in the living body whereas, natural selection brings both phenotypic and genotypic variations.

Mutation is a type of microevolution that happens several times over many generations causing huge variations.

Natural selection is a type of macroevolution that takes more than thousands of years to happen.

Hardy-Weinberg equilibrium states that when no population is evolving, then the allele frequencies will stay the same across generations.

So, both Mutation and Natural Selection are the mechanisms of evolution that violate the Hardy-Weinberg equilibrium. Thus, stating that they both can together cause evolution.

2. Both Mutation and Natural Selection leads to adaptations

Any type of evolutionary change deserves that the organism is better changed or altered both phylogenetically and genetically in order to better fit its environment. So, this is controlled by adaptations.

In the evolutionary theory of mutation, adaptation is defined as the introduction of new beneficial variation that has a positive effect on the fitness of the offspring.

Mutation can cause both beneficial and harmful types of variations over time. The harmful variations lead to death or extinction in the population, whereas beneficial variation can cause adaptations.

In the evolutionary theory of natural selection, adaptation is defined as the biological mechanism by which organisms adjust to new environments or in their current environment in order to survive and reproduce.

Natural selection means that adaptions occur naturally without any artificial involvement. When the organism finds it very hard to live in its habitat it develops various ways phylogenetically and genetically to make its survival a lot easier and that’s adaptation.

3. Both Mutation and Natural Selection leads to speciation

We have previously learned that mutation is a microevolutionary concept whereas, natural selection is a macroevolutionary concept.

It’s because the mutation is a small-scale evolution that leads to changing a few genes leading to the creation of new alleles within a population. This leads to the change in allele frequencies in a gene pool.

Whereas, natural selection is a very large-scale evolution that results from the sum total of all of the mutations (microevolutions) that took place within a population. This can lead to the formation of new species i.e speciation.

Therefore, it is very clear that both mutation and natural selection helps in adaptation which is beneficial to the organism and its population.

And when successive adaptations take place it leads to the formation of new species from the ancestral ones either by way of convergent evolution or divergent evolution, which is also called speciation.


Degeneration

Mutations mean that humans are headed for extinction, along with all other organisms.

We started talking about maintenance mishaps&mdashthe proper term in biology is mutation&mdashcopying mistakes in our DNA (note that not all genetic changes are copying mistakes, some can be designed adaptive changes, as discussed above). These copying mistakes are accumulating at such a high rate that we can&rsquot get rid of them (see Mutations: evolution&rsquos engine becomes evolution&rsquos end!). This is called genetic entropy. We produce up to 100 new mutations per person, per generation. That means I have up to 100 more mutations than my Dad, and my son has up to 100 more mutations than me. The key however, is that children will always have more copy mistakes than the parents, never the same amount or less. This means natural selection would have to get rid of all the children to keep mutations out of the population to avoid extinction. So the end result of avoiding extinction would be &hellip extinction. To make matters worse, the individual effect of most mutations is so small that natural selection can&rsquot even &lsquosee&rsquo them to get rid of them. Actually, we&rsquove got way more chance of dying by dumb &lsquoluck&rsquo than we do of dying by natural selection. And even if someone manages to get a good mutation, that mutation can&rsquot be separated from the much more common bad mutations, so their effect gets drowned out amid all the bad noise (see The diminishing returns of beneficial mutations). What does all this mean? It means the human race is doomed to extinction, and we can&rsquot do a thing about it. And it&rsquos not just humans either. All life is doomed to the same fate! (see Genetic entropy and simple organisms) Extinction is our future, not evolution.


Revolutionary Ideas: Darwin and Wallace

Photo of Alfred Russel Wallace (left) and Charles Darwin (right), co-discoverers of natural selection.

A New Paradigm Emerges: Darwin and Wallace

Scientific discovery often occurs over time, but always occurs through the accumulation of data. Thomas Kuhn (1962) outlined how scientific “revolutions” are structured as changes in a paradigm. A paradigm is a pattern of thinking. Old models and theories give way and evolve as new information arises. Sometimes, the entire pattern of thinking shifts in a major way, marking an entirely new way of approaching scientific problems. Charles Darwin and Alfred Russel Wallace both discovered, pretty much at the same time, the key process that would lead to a new paradigm in evolution. This key process was natural selection, the variation in survival due to advantages and disadvantages in certain traits within an organism. Before Darwin and Wallace, Linnaeus’ ideas showed the relatedness of life and Lamarck’s ideas about inheritance supposed that life has changed over time. These ideas represented the paradigm of the time. Darwin’s publication of “The Origin of Species” in 1859 initiated a major shift in the view of how traits are transmitted from parent to offspring. Rather than parents passing traits directly to offspring through use or disuse, Darwin and Wallace would argue that this occurred through natural selection. Their views on this were influenced by two major factors. First, Thomas Malthus’ writings on economic ideas regarding population and resources emphasized that population growth eventually far outstrips available resources in an environment. Second, both Darwin and Wallace had opportunity to conduct extensive fieldwork in locations filled with biodiversity relatively untouched by intensive human development.

Charles Darwin famously spent five years (1831-1836) as a naturalist aboard The Beagle, a British ship with a mission to circumnavigate the globe. During this time, Darwin was able to spend extended periods of time on land, exploring regions around the South American coast, from Brazil to the Galapagos and beyond. He collected rocks, fossils, animal specimens, planet specimens, and more. Sending them on to England prior to his return, these collections made him famous and would become his life’s work. Ultimately, the immense variation in plant and animal species across South America was puzzling. He found many completely different species living in environments that were very similar. Why was there such variation across distances if the environments were so similar? The classic example of this are his observations of finch variation across the Galapagos Islands (Darwin’s Finches). The best way to characterize this variety was by invoking a common ancestor sometime in the past that, as its descendants moved from island to island, evolved into new species. Another example from his voyage came from his explorations of the greater rhea and lesser rhea, two flightless birds that local guides often ate as food in the area around Bahia Blanca, Patagonia. These two birds were very similar, but different species. Because one lived north of the Rio Negro (River) and the other south, their ancestors must have pursued separate evolutionary trajectories. Darwin’s insights were not relegated only to living specimens. Darwin also collected many fossils. In subsequent study back home, he made connections between his living specimens and fossil ancestors. Such evidence would become very important for the development of his ideas around natural selection.

Stops along Charles Darwin’s second voyage of “The Beagle” (1831-1836). These includes locations from Australia to Cape Town, South Africa, to South America and, eventually, back to England.

Alfred Russel Wallace conducted most of his work in two places. Like Darwin, he spent a great deal of time in South America, particularly Brazil. He also conducted field work in what is today Malaysia, Indonesia, and nearby places. Inspired by the field work of Darwin and others, he funded his expeditions, running between 1848 and 1862, through the sales of collected specimens. He methodically planned his field work to explore ideas he had surrounding biogeography, or the geographic distribution of species. If evolution occurs, he reasoned, closely related species should live close to one another. His field work played this out, noting that rivers and other bodies of water did indeed separate related but distinct species. His classic example, called the “Wallace Line,” notes the separation of species of Asian and Australasian descent by the Sunda Straits.

Map of Indonesia, Australia, and environs depicting “Wallace’s Line”. This line between landmasses separates Asian from Australasian faunas and was described by Wallace. The differences in species across this line provided Wallace with the patterns he used to describe his views on natural selection and evolution.

He noted that while some species likely descended from a common ancestor had evolved very differently on either side, certain species of flora were the same on both sides. These straits being about 35 km in width, the mobility of an organism was key. Plant pollen and seeds, blown by the wind or transported by water, allow growth on both sides of the strait. Large mammals and most birds, by contrast, could not traverse it. This separation, over time, would lead to new species where once an ancestral form existed. At the time, Wallace would not have known what we now know about the role of plate tectonics in this biogeographical separation. But, he was able to correctly observe here, and elsewhere in his work, that biological change occurs as new species arise from prior species. He recognized natural selection as the mechanism for these observations. Favorable traits, or traits that gave organisms an adaptive advantage, were retained while unfavorable traits would make organisms unfit for their environments.

The two men did correspond. While Darwin came to the idea before Wallace, it was in conversation with Wallace that natural selection, and the new paradigm that would follow, emerged. In 1858, they jointly read papers at a meeting of the Linnaean Society, which would mark the first public description of evolution through natural selection. This was followed one year later by Darwin’s publication, On the Origin of Species. Darwin and Wallace described natural selection as the mechanism that makes survival to the next generation possible, though it does not mean that these offspring are necessarily the “fittest” to survive. Organisms just have to have enough favorable characteristics to be able to survive long enough to pass on their genes, in whatever condition, on to the next generation. Sometimes, genetic mutations passed on are benign. Other genetic changes passed on provide a favorable adaptation for offspring. At still other times, mutations passed on are detrimental to the survival of offspring or even the ability of a parent to reproduce at all.

Meanwhile, Back in Europe: Mendelian Inheritance and Genetics Take Shape

Even with this new understanding of natural selection, it would take an understanding of how genes work to explain how they are inherited by offspring. The foundations for understanding inheritance would come from the 1860s work of an isolated monk in a Czech monastery. While Darwin and Wallace toiled around the globe and in the heat of rainforests, an important part of evolutionary theory was taking shape through humble pea plants. Gregor Mendel, the son of a farmer, was very interested in plants. Harnessing his curiosity and focusing on pea plants, he crossbred a wide array of varieties and recorded how traits were passed down in the next generation. Applying his mathematics training, Mendel was able to use statistics, applied to his pea plant populations, to predict which traits – smooth skin, wrinkled skin, and so on, would be inherited. As is often the case with new scientific insights, this work was not recognized for its importance right away. But, owing to the work, interests, and curiosity of this isolated monk, natural selection was bolstered with genetics. Natural selection would not only be attributable to environmental factors, but could now also be described by changes in how genes are inherited from one generation to the next.

Characteristics of pea plants Mendel used in his inheritance experiments. These include seed form, cotyledon color, flower color, pod form and color, flower position on stem, and stem size. Mendel’s laws of inheritance. (I will recreate this. I found it and it’s okay, but I want to remove Mendel and the green arrow at least because it’s redundant and doesn’t really fit.)

There are three principles in Mendelian genetics. It is also worthy to note that, though the term “Laws” here are accepted within the scientific community, there is enough deviation from them that they may be more accurately referred to as “Principles.” Genes come in two forms called alleles (“Law of Segregation”). Alleles can be dominant (expressed in an organism’s appearance) and recessive (not-expressed). This is the “Law of Dominance”. You may remember creating Punnett Squares in a previous biology class – as these are a tool that can be used to analyze the expression of one allele over another from one generation to the next. The selection of one allele of a gene over another, however, occurs independently of selection occurring among other genes (“Law of Independent Assortment”). These laws, however, do not describe how one allele is transmitted to the next generation, only that alleles exist, are treated independently of other genes during selection, and ultimately determine what variants of such genes are physically expressed. For instance, there are cases where one allele is not completely dominant over another, a situation called “incomplete dominance”. Likewise, there are situations where the phenotype for both alleles is expressed. This is called “codominance”. It is also known that some genes exist in nature with more than two alleles, or “multiple alleles”. Finally, some traits are actually “cogenetic”, such as the color of fruit fly eyes, where several genes contribute to a physically expressed variation.

Fruit fly specimens displaying eye color variation.

Mutation, Migration, Drift, and Natural Selection

There are several key processes that drive evolutionary change at all scales. These are genetic mutation, gene migration, genetic drift, horizontal gene transfer, and natural selection.

Genetic mutations are simply changes in the sequence of nucleic bases in the coding portion of a DNA molecule. These can be caused by errors in replication or repair of a sequence as it is passed on to the next generation.

Gene migration, or gene flow works differently. Sometimes, a new, sexually reproducing, individual from a separate population is introduced into a new population of the same species. Introduced traits can include many things, such as new varieties of colors within an insect population. This new and unique genetic material mixes into the descendant populations and can then lead to unique and novel down-generation changes. Genetic material can also be exchanged with the donor population in the same manner as populations subject to gene migration are not necessarily isolated.

Gene flow, the transfer of alleles across populations, is depicted here showing birds from two populations living on either side of a mountain. Species A, the blue birds, contains the dominant alleles while species B, the red birds, contain the recessive alleles. A member of species A is able to incorporate it’s allele for blue color into the red population through mating. This is one way that gene flow can work (Jessica Krueger, Wikimedia Commons CC BY-SA 3.0)

Genetic Drift does not lead to adaptational changes in a population. Rather, it is the result of chance, most commonly because some individuals have left behind more offspring than others. It is a change in the frequency of an allele over time, and is completely independent of environmental changes. The genes of the following generations were passed on by those of the individuals fortunate enough to reproduce successfully, and not necessarily of the “fittest”. One simple example comes in populations reduced to small numbers that then recover, such as the American Bison, which was nearly hunted to extinction. While its population is much larger than in the past, its genetic variation is much lower than it was 200 years ago (Ungerer et al., 2012). A simpler example might come among a human couple, each with different eye colors, say brown and blue, but where brown represents the dominant allele. Even if the chance of having brown eyes is 50%, all children may statistically end up with blue eyes, thereby eventually erasing that dominant allele. Such cases provide excellent examples of where phrases like “survival of the fittest” are at best an oversimplification of evolutionary processes.

An example of genetic drift using rabbits. Genetic drift allows for the removal of an allele from a population due to chance. Even through the allele frequency for brown and white fur coats is equal in the first generation, the dominant allele (for a brown coat) quickly displays with more frequency in subsequent generations, eventually eliminating the recessive trait for white coats.

Two other important evolutionary mechanisms that also occur at the genetic level, but in different ways, are horizontal gene migration and genetic symbiosis. Gene transfer, as we usually think of it, is vertical. This means that genetic material is transferred from parent to offspring. Horizontal gene transfer occurs sideways (Figure left), as with viral transfer. It also occurs among bacteria and archaea that have no means of sexual reproduction. Most of us are familiar with viruses, as we suffer from them frequently and, if we are responsible and had responsible parents, have been vaccinated against them wherever possible. Bacteriophages are a kind of virus that replicates within bacteria and holds promise toward fighting antibiotic resistance (Bragg et al., 2014). Because they inject their genome into host cells where it can replicate, viruses are able to transfer DNA from related and unrelated organisms. This method of transfer is called transduction. Plasmids, which most often are transferred horizontally via a process called transformation, are genetic material that exists in a cell independent of chromosomal interaction. Transformation is the transfer of genetic material between cells. The final method of horizontal transfer, which can occur via the transfer of plasmids or transposons (a chromosomal segment that can undergo a change of location), is conjugation, which occurs through direct physical contact between cells. Genes can also be transferred horizontally through gene symbiosis, which results from close ecosystem interactions between, at times, species that are evolutionarily separated a great deal. Endosymbiosis is thought to be the origin of key eukaryotic organelles such as mitochondria and chloroplasts (each of which brought its own DNA with it into the host cell). Fungi may transfer genetic material to an arthropod, such as an aphid, through exchanges of cellular material from close physical interactions. In any of these situations, horizontal gene transfer is very difficult to measure, but is also a key evolutionary mechanism that maintains diversity and novel mutation.

Horizontal gene transfer as a form of inheritance, in this case through the transfer of genetic material across Kingdoms through plastids and mitochondrial materials (Smets, 2005).

So far, all of the mechanisms of evolution discussed have been random in nature. Our final mechanism, natural selection, is very much not random. The genetic mutations produced by drift, horizontal migration, and others simply make an organism fit into its environment differently, which can lead to being passing such genes along or not. For natural selection to work, there are a number of important requirements that must be met. Within a population, there must be enough genetic variation to provide the flexibility necessary for advantageous mutations. There must also be a system of heredity that allow offspring to inherit the genes of the parents. Ultimately, a population will necessarily experience differential reproduction, where not all individuals will survive to reproduce due to environmental pressures. These can be everyday pressures, such as predation, that exist in periods of environmental calm, or stasis. They can also occur as a result of rapid environmental change, such as a local volcanic eruption, an extinction-triggering asteroid impact, or our modern episode of anthropogenic climate change. Natural Selection assures that the individuals who survive are more likely to pass on their genes.

Forms of Natural Selection

Some of the most amazing, flamboyant, and beautiful things in the biological world are the result of sexual selection. Sexual selection is where a species uses physical features or physical prowess to gain the opportunity to mate with another and pass on their genetic material. Peacock tails, colorful feathers on many male birds, and even dancing among fruit flies can inspire attraction of the opposite gender. Such things grab attention! Sexual selection can also produce situations that are very detrimental to a long life. Organism can become more susceptible to predation. Such selection can require the organism to give up its life in order to pass on these genes. Examples of the latter include sexual cannibalism in male black widow spiders or in some species of mantids where sperm is not released until the male’s head has been removed. In these mantids, this form of sexual selection may even be the main driver in the evolutionary change observed in their genitalia (Jensen et al., 2008).

Artificial Selection has been used for agriculture for thousands of years, as our species has continued to select for what are seen as favorable attributes. A classic example is the development of corn, or maize. Today, it is such a staple grain in our diet that you can find a corn product in nearly any food you purchase that has been processed. This includes meats, as many livestock are fed corn-based diets, even if they are not evolved to consume it well, such as with cattle. Native to Mesoamerica, the teosinte grass was used for its kernel and, over time, plants with plumper kernels were selected, eventually leading to the corn we see today. This form of plant domestication, an indigenous American export to the world, is now a staple everywhere.

Teosinte development through artificial selection, or domestication, significantly increased kernal volume and number over time (By John Doebley, Wikimedia Commons)

Another critical example of artificial selection, or domestication, that has shaped the modern world in particular came from Normal Borlaug’s work on wheat. Where ancient mesoamericans were selecting for corn based simply upon the appearance of a kernel, Borlaug, as a microbiologist, would select wheat strains based upon their DNA. The problems he was addressing with wheat were directly related to a need to increase yield, shorten the stem of the grain to improve its ability to hold up until harvest, and to make it more disease resistant. Through the use of genetics, this work addressed these problems in the short span of 20 years. The results are still being experienced by people around the world today, through their ability to feed many more people than would have been possible otherwise (nobelprize.org, 2019). There are myriad examples of human-driven artificial selection that have resulted in the food we eat today. Artificial selection works by humans purposefully choosing individuals that will reproduce, based on which ones have characteristics valued by the farmer or researcher.

Coevolution

There are many examples of situations where two or more species will, as time passes, environments change, and natural selection occurs, affect one another’s evolutionary trajectory. Most often, these occur through ecological relationships. These relationships can be mutually beneficial, competitive, predatory, or parasitic. Coevolution is common in nature and illustrates the web of complicated relationships that allow the biosphere to function.

A classic example of coevolution is one that we rely on daily, the interaction between flowering plants and pollinators, such as honeybees. Such coevolutionary relationships are mutualistic, meaning that both species benefit from the interaction. The bees gain food while the plants are able to spread their pollen. Another excellent example of coevolution exists between the acacia ant, Pseudomyrmex ferruginea and the various species of the genus vachellia, acacia, that it protects. The ant is an obligate organism, in that this form of mutualism is absolutely necessary for its ability to reproduce. The acacia plants provide food and thorns that serve as nests while the ants protect the acacia from herbivores. Such examples are not limited to the world of the living. The fossil record even bears out examples. A fabulous one, depicted in the image below, shows a platycerid snail fossilized near the anal vent of a crinoid. There are actually quite a few examples of this particular relationship, which suggests that it was quite normal for these snails to feast upon crinoid poop!

Coprophagus, or the eating of feces, by a Platycerid snail lodged near the anal vent of a crinoid. Ordovician, Kentucky (Rich Schrantz, 2000).

A Word About “Fitness”

Genetic change within populations acts randomly. Natural selection makes it more probable that individuals who are genetically prepared for current or new environmental realities will survive. They are the ones most likely to pass on the genes coded for the traits which permit survival. While genetic changes are random, natural selection is most definitely not random. Adaptations that make an organism fit for a cold climate, such as fur on a polar bear, will not likely be advantageous when that climate warms again at some point in the future. Staphylococcus aureus, a purveyor of infection throughout the human body, was famously stopped by the antibiotic Penicillin, developed by Alexander Fleming early in the last century. S. aureus roared back rapidly with resistance a few short years later and has now become so resistant to antibiotic treatment that some strains, such as “Methicillin-resistant S. aureus” (MRSA) are now feared in hospitals, where community infections can spread rapidly among healthy individuals (Chambers and DeLeo, 2010).

Fitness is a situational circumstance, dependent upon being “good enough” for the environmental conditions of the moment, not the ability of an individual to “pull themselves up by their bootstraps”, or run a marathon, or win in a fight, providing themselves some kind of position of advantage through their own will. Ultimately the fitness of an individual is expressed by adaptations, or features that provide some improved function in an environment that is produced through natural selection. There are many features, it should be noted, that are not adaptations. These include vestigial structures, non-functional adaptations left over from an ancestor. Another example of a non-adaptive trait includes the red color of your own blood, which is a result of its chemistry and not due to some kind of selection. Exaptations make up another category. These are features that may have formerly had an adaptive purpose, but was not produced by natural selection for its current use. These can also be both physical and behavioral. One behavioral exaptation example might be domesticated dogs licking the mouths of their mothers. Interpreted as a means to get a parent to regurgitate food for them, this same behavior in wild wolves toward a lead wolf is interpreted as showing submissiveness (Bauer and Smuts, 2007).

Some traits can also be maladaptive, or harmful to a species fitness. A 2019 study released by Pagano et al. suggests that the eustachian tube construction in Neanderthal humans, Homo sapien neanderthalensis, made it susceptible to ear infections. Their reconstruction of the neanderthal eustachian tube suggests that its horizontal construction, very similar to human infants, may very well have even contributed to their eventual extinction. Human infants are notoriously susceptible to ear infections because of this construction of the tube, which can lead to pneumonia and, if left untreated, even death. As infants grow toward adolescence and adulthood, the eustachian tube does not remain horizontal, allowing drainage to occur and less likelihood of infections. Interestingly, while many of us (particularly of European descent) carry neanderthal genetic variants within our genome, given that our our two sub-species are known to have interbred thousands of years ago, it is likely that this eustachian tube, arguably maladaptive in neanderthals, is a trait derived from a common ancestor. Ultimately, this trait may have reduced fitness for our nearest human cousins while remaining a relatively benign feature for our own species.

Modern Evolutionary Theory: “The Modern Synthesis”

The combination of Darwinian ideas with Mendel’s genetics is referred to as the “Modern Synthesis”. This term was coined by Julian Huxley in his 1942 book, “Evolution: The Modern Synthesis”. Tying in malthusian ideas about population genetics with evolutionary theory, Huxley provided a framework that effectively brings together the macroevolutionary changes seen in the fossil record with the microevolutionary changes observed in nature and laboratories. However, this revolutionary model also provided the foundation for the rapid biological advances that would occur during the latter half of the 20th and into the 21st centuries. Some of these later developments and discoveries, such as horizontal gene transfer, developmental biology and embryology, etc. have yet to be fully integrated within this framework. Rather than totally replacing the modern synthesis with something new, work continues to discover ways to integrate such new fields and discoveries, ultimately towards finding a way to unite these ideas into a unified, single model. This can be referred to as neo-Darwinian evolutionary theory.

Diagram of the Modern Synthesis of evolutionary theory. The combination of principles undergirding population dynamics with understandings from genetics is synthesized into a larger and more coherent model of how organisms and populations evolve.


Darwin's God

A child once informed his friends his toy bulldozer could dig all the way through the Earth. But wasn’t the Earth too big? No, look at the Grand Canyon—it is proof of what such small shovels can do. Such childish logic, amazingly, shows up repeatedly in evolutionary “theory.” It is a treasure trove of bizarre and silly claims and justifications which rises to the surface, as with the child’s reasoning, when the evolutionist is questioned about his convictions. Consider, for example, the oft heard evolutionary mechanism of random mutation followed by natural selection which, like the toy bulldozer, apparently can do just about anything. When queried about this most amazing idea, the underlying evolutionary logic is revealed.

One response evolutionists give when confronted with their own extraordinary claims about random mutation and natural selection is to complain that mutations aren’t really random, and any such notion is clearly erroneous. They don’t just happen willy-nilly but in fact reveal non random patterns both across the genome and across time.

But this is an equivocation on the word “random,” which is used with reference to something. When evolutionists speak of random mutations, they mean that the mutations are random with respect to the need of the organism. There is no plan or intelligence behind mutations—evolution has no final causes.

When questioned about their bizarre claim that the entire field of biology is a consequence of such Lucretian bloopers, their rebuttal that mutations actually aren’t random after all reveals how shallow is their thinking.

Evolutionists are the ones who claimed mutations are random (with respect to the need) and the fact that mutations are not random over space and time does not change that Epicurean claim. (By the way, this is yet another evolutionary expectation that turned out to be false. That became clear when the empirical evidence caught up with evolutionary speculation.)

Another response evolutionists give when questioned about their startling ideas of the power of random mutation and natural selection is to focus on the latter. Mutations may be random but evolution certainly is not, for selection pressure brings out the winners.

Of course this is false. Selection “pressure” is another evolutionary euphemism. The only thing Darwin’s natural selection can do is kill off the faulty or inferior designs—it does not induce helpful mutations to magically arise. All evolutionary creations must arise from those random mutations.

Yet another revealing response evolutionists give when queried about their heroic claims of random mutation and natural selection is to complain that such a query is nothing more than a strawman rendition of evolution.

Random mutations, after all, are only one of a great many evolutionary mechanisms. One professor has listed almost fifty different so-called “engines of variation” that work together to build biology’s wonders. How silly to think random mutation was the sole artist in Darwin’s montage.

For example, biological variation can arise from changes in the expression levels of genes, which in turn can arise from changes to sequences that control such expression levels, or changes to the protein machines that bind to those sequences. And there are far more involved examples, such as the various forms of symbiotic mechanisms. The professor concludes:

But does this really rescue random mutation from its overachiever status? No. Once again the evolutionary logic has bubbled up to the surface for all to see. The most obvious problem here is simply that biology’s various engines of variation are, according to evolutionary mandate, ultimately the product of, yes, random mutation.

Of course RM/NS is the ultimate explanation for evolutionary change. The fact that biology reveals incredibly complex adaptive and physiological changes does not give evolutionists license to invoke them as evolutionary starting points, without reference to their own origin.

Indeed, with evolution what we must believe is that its blind mutations just happened to create phenomenal mechanisms which, themselves, not only are astonishingly complex but become crucial agents of evolutionary change. The heroics continue to mount at an astronomical pace as evolution, we must believe, creates evolution. If a toy bulldozer can dig through the Earth, then why not?

243 comments:

This comment has been removed by the author.

Given enough time (20 million or so years) and enough flow, even something as soft as a Colorado River could carve out something as long and wide and deep as the Grand Canyon.

Unless one considers the earth to be less than 10,000 years old.

So the kid was on to something.

One can try to look intelligent by making claims that could never be proven.

Excellent post. However, in Evolution theory, not only the mutations are random but also the selective pressure.
It's a bit like a casino roulette game. The ideas that only mutation is random is like to put your money on a number, let say 9, and then to play until the ball fall on a 9. On the other hand, in reality, in evolution not only the mutations are random but the selective pressure too. In the casino roulette game, it's a bit like changing randomly numbers (from 1 to 10000 for example) and hoping to get the ball falling on the same number (even though the ball can only fall on numbers between 1 and 37).
It's much much more unlikely.

I like the comparison of evolution to the toy bulldozer. but don't you think you are being to generous even with a toy bulldozer as to what RM & NS can actually do in reality?

As former president of the French Academy of Sciences Pierre P. Grasse has stated:

“What is the use of their unceasing mutations, if they do not change? In sum, the mutations of bacteria and viruses are merely hereditary fluctuations around a median position a swing to the right, a swing to the left, but no final evolutionary effect.”

Scientists Discover What Makes The Same Type Of Cells Different - Oct. 2009
Excerpt: Until now, cell variability was simply called “noise”, implying statistical random distribution. However, the results of the study now show that the different reactions are not random, but that certain causes (environmental clues) lead to predictable distribution patterns.
http://www.sciencedaily.com/releases/2009/09/090911204217.htm

Revisiting The Central Dogma (Of Evolution) In The 21st Century - James Shapiro - 2008
Excerpt: Genetic change is almost always the result of cellular action on the genome (not replication errors). (of interest - 12 methods of information transfer in the cell are noted in the paper) http://www.uncommondescent.com/intelligent-design/central-dogma-revisited/

Random Mutations Destroy Information - Perry Marshall - video
http://www.metacafe.com/watch/4023143

Mutation Studies, Videos, And Quotes
http://docs.google.com/Doc?docid=0AYmaSrBPNEmGZGM4ejY3d3pfMjZjZnM5M21mZg

This comment has been removed by the author.

This comment has been removed by the author.

"One response evolutionists give when confronted with their own extraordinary claims about random mutation and natural selection is to complain that mutations aren’t really random, and any such notion is clearly erroneous."
-Which Evolutionist ever claimed that Mutations are not random ?
Of course Mutations are random and I would be surprised to see even one Biologist claiming something different. How did you get such a strange idea ? Is it the existence of mutational hotspots ? (If so, read up on the definition of "randomness" - it does in no way imply a uniform distribution of events)
Or is it the sometimes observed increased mutation rate under stress in certain organisms ? (If so, think again - the rate of mutations has nothing to do with Mutations being stochastic or deterministic events).

And this sentence:
"Of course this is false. Selection “pressure” is another evolutionary euphemism. The only thing Darwin’s natural selection can do is kill off the faulty or inferior designs—it does not induce helpful mutations to magically arise."
is more than strange. Could you please quote even one Biologist who ever argued that Natural selection helps beneficial mutations to *ARISE*.

Andreas: [Q]uote even one Evolutionist who ever argued that Natural selection helps beneficial mutations to *ARISE*.

I had no trouble understanding what Dr. Hunter meant. The word "pressure" in selection pressure implies a cause and effect relationship. That is, there is a force in nature that causes mutations to occur, and maybe even certain kinds of mutations to occur.

Obviously that is not the case, and that is why "selection pressure" is really a poor term to use.

As I have read the evolutionary literature I have become acccustomed to the use of the active voice. None of it can be taken literally it is merely a convenient way of expressing oneself.

For example, "the only thing natural selection can do is kill off faulty or inferior designs."

What does this literally say. There is an active force in nature that has the ability to detect faulty designs and kill the organism that possesses them. Is this really what happens?

The subject was the toy bulldozer, not water. We know that water is one of the most effective solvents known. You missed the point, but it shows how in your thinking you are able to jump from one to another without making distinctions. This kind of "jump thinking" for lack of a better term is unjustified and seems to be a common trait among evolutionists. What is needed is more critical and focused thinking to turn someone away from the evolutionary fairy tales.

Tough questions an evolutionist needs to ask themselves:

1. What do I really know for sure about evolution?

2. What's the bottom line as far as what we actually have observed empirically about evolution?

3. What is the contrary evidence?

This comment has been removed by the author.

@Doublee:
"Obviously that is not the case, and that is why "selection pressure" is really a poor term to use."
- Cornelius did not complain about "selection pressure" being a poor choice of words (which it might be). He wrote ". it does not induce helpful mutations to magically arise" which is something that no Evolutionist ever claimed.

"What does this literally say. There is an active force in nature that has the ability to detect faulty designs and kill the organism that possesses them. Is this really what happens? "
- Imagine a population of bacterial cells with some individuals being resistant to Penicillin. If Penicillin is present in the environment, those individuals that are resistant are much more likely to reproduce than the individuals that are not resistant - which causes the allele(s) mediating resistance to penicillin to spread in the population. Whether you call this process an "active force" (how would you define this term ?) or not is mere semantics.

List Of Degraded Molecular Abilities Of Antibiotic Resistant Bacteria:
http://www.trueorigin.org/bacteria01.asp

Is Antibiotic Resistance evidence for evolution? - "The Fitness Test" - video
http://www.metacafe.com/watch/3995248

Testing the Biological Fitness of Antibiotic Resistant Bacteria - 2008
http://www.answersingenesis.org/articles/aid/v2/n1/darwin-at-drugstore

Thank Goodness the NCSE Is Wrong: Fitness Costs Are Important to Evolutionary Microbiology
Excerpt: it (an antibiotic resistant bacterium) reproduces slower than it did before it was changed. This effect is widely recognized, and is called the fitness cost of antibiotic resistance. It is the existence of these costs and other examples of the limits of evolution that call into question the neo-Darwinian story of macroevolution.
http://www.evolutionnews.org/2010/03/thank_goodness_the_ncse_is_wro.html

Neal "liar for Jesus" Tedford said.

Tough questions an evolutionist needs to ask themselves:

1. What do I really know for sure about evolution?

That it happens, and has been happening for at least the last 3.3 billion years. Many if not most of the mechanisms of evolution are known, although there is still work to be done on specific details.

2. What's the bottom line as far as what we actually have observed empirically about evolution?

Bottom line is we have over 150+ years of cross correlating and corroborating positive evidence from hundreds of different scientific disciplines supporting evolution. As an explanatory framework for observed biological phenomena it has never been seriously challenged.

3. What is the contrary evidence?

There are plenty of possible ways to falsify ToE, but to date none have been found.

Tough questions an evolutionist needs to ask themselves:
1. What do I really know for sure about evolution?
2. What's the bottom line as far as what we actually have observed empirically about evolution?
3. What is the contrary evidence?

Tough question Neal must ask himself,

"If I am so confident that the theory of evolution is vacuous, why am I asking these "tough questions" on some obscure blog instead of confronting scientists at the university in my neighborhood?"

Great post Cornelius. This toy bulldozer idea of course leaves out things like gigantic subterranean granite boulders. Evolution likewise doesn't factor in bad mutations that aren't enough for selection to filter out but build up over time. The vast, vast majority of observed mutations bad. John Sanford compares the "good" mutations to bailing out a sinking boat with a Dixie cup.

What One Famous Scientist Said About Evolution.

"One morning I woke up and something had happened in the night, and it struck me that I had been working on this [evolution] stuff for twenty years and there was not one thing I knew about it. That's quite a shock to learn that one can be so misled so long. Either there was something wrong with me or there was something wrong with evolutionary theory. Naturally, I know there is nothing wrong with me . "

"[The] question is: Can you tell me anything you KNOW about Evolution? Any one thing? Any one thing that is true? I tried that question on the geology staff at the Field Museum of Natural History and the only answer I got was silence. I tried it on the members of the Evolutionary Morphology Seminar in the University of Chicago, a very prestigious body of Evolutionists, and all I got there was silence for a long time, and eventually one person said, "I do know one thing - it ought not to be taught in high school"."

—Part of a keynote address given at the American Museum of Natural History by Dr Colin Patterson (Senior Paleontologist, British Museum of Natural History, London) in 1981. Unpublished transcript.

you can get the audio transcript of the Patterson quote here:

@bornagain77:
I would always be careful with such quotes, see for example:
http://www.anevolvingcreation.net/collapse/examine.htm

Also, for the sake of fairness, lets consider what Mr. Patterson thinks about Creationists quoting him:
"I was too naive and foolish to guess what might happen: the talk was taped by a creationist who passed the tape to Luther Sunderland. Since, in my view, the tape was obtained unethically, I asked Sunderland to stop circulating the transcipt, but of course to no effect. There is not much point in my going through the article point by point. I was putting a case for discussion, as I thought off the record, and was speaking only about systematics, a specialized field.
I do not support the creationist movement in any way, and in particular I am opposed to their efforts to modify school curricula. In short the article does not fairly represent my views. But even if it did, so what? The issue should be resolved by rational discussion, and not by quoting 'authorities,' which seems to be the creationists' principal
mode of argument." (Letter from Colin Patterson to Steven W. Binkley, June 17, 1982)."

You're quite fond of the worst kind of argument from authority: one that deliberately mis-quotes authorities who believe the opposite of the quotemine!

You haven't apologized for the last egregious run of quotemined, falsely attributed, and in some cases, fully made up quotes you spewed out here, and I debunked. Do we really need to go through this again?

"I was too naive and foolish to guess what might happen: the talk was taped by a creationist who passed the tape to Luther Sunderland. Since, in my view, the tape was obtained unethically, I asked Sunderland to stop circulating the transcipt, but of course to no effect. There is not much point in my going through the article point by point. I was putting a case for discussion, as I thought off the record,
and was speaking only about systematics, a specialized field. I do not support the creationist movement in any way, and in particular I am opposed to their efforts to modify school curricula. In short the article does not fairly represent my views. But even if it did, so what? The issue should be resolved by rational discussion, and not by quoting authorities,' which seems to be the creationists' principal mode of argument." (Letter from Colin Patterson to Steven W. Binkley, June 17, 1982)."

Are you ethically challenged?

Oops, Andreas beat me to it.

Add to add the ethical abuse, the creationists are now SELLING the audio transcript. Look at the bottom of BA's link. Turn a profit on a unethically obtained secret taping.

You know in many states it is even illegal to tape without permission of all parties?

This is an interesting point. That is quite the contradiction. To use the word 'random mutation' is intentionally injecting dogma into science. i.e. 'random' = no need for design or a designer.

I'm no scientist, but I am curious about another apparent contradiction. Life is resilient, and it springs up at every possible opportunity, in the most extreme and hostile environments. We are currently looking for water on the Moon and Mars to prove that there once was life. And NASA et al seem to think that once you have water - boom – LIFE wuz there. How does this not totally contradict the dominant paradigm? Evolutionists don't have biogenesis, but they claim they know the approximate conditions in which it happened all on its own. How can both of these things be true? How can in one hand we look for life by just looking for signs of water, and in another situation say you need all of these conditions to be juuuuuust right to make it spring out of nowhere?

I'm sure I could frame my question better. Ultimately, this is a mine field for the evolutionist in my opinion. For an evolutionist to use life’s resilience as proof that we don’t need a creator is absurd. Life is pre-programmed to be resilient. It’s not randomly resilient.

To use the word 'random mutation' is intentionally injecting dogma into science. i.e. 'random' = no need for design or a designer."

No. We observe the nucleotide changes are actually random. For example, we can sequence a gene of bacteria, or a human, through generations. We observe the accumulation of random changes. Some don't even change the amino acid sequence. So they appear random-hitting the genome at random positions, with measurable frequency.

And yet Patterson said the words denigrating evolution with full intent of the meaning behind it. i.e. it is a "in context" quote and is not misleading, though the wording is not exact to the transcript, so it seems you guys have merely agreed that the truth of the emptiness of evolutionary theory should be hidden under the rug and find it unethical that creationists would want to reveal the truth of the extreme vacuous nature of evolution. Thus it seems that if a creationists says evolution is full of hot air you will simply ignore it because he is a ignorant "creationist", yet if a leading evolutionist is caught airing full blown doubt of evolution in front of a audience full of other leading evolutionists it is considered unethical because. because. because he did not want to be embarrassed for revealing the truth? How convenient for you guys to lecture me on ethics so as to preserve the lie/religion of evolution.

"The entire field of biology is a consequence of such Lucretian bloopers"

Lucretian blooper huh? De rerum natura? Are you arguing it is a fundamental error to even try to describe the universe in natural terms? Death to science, long live superstition?

Funny, considering the other day you said:
"There's nothing wrong with MN in biology or any other area of science."

What kind of methodological naturalism considers the supernatural? Isn't MN a Lucretian blooper?

"Another response evolutionists give when questioned about their startling ideas of the power of random mutation and natural selection is to focus on the latter. Mutations may be random but evolution certainly is not, for selection pressure brings out the winners."

You've got it. We observe the accumulation of mutations in the genome. They are random with respect to need. Their persistence in a population is not.

"Of course this is false. Selection “pressure” is another evolutionary euphemism."

Ehh? Euphemism? Pressure is perhaps a throw away word-selection suffices. Are you denying selection can and does occur?

"The only thing Darwin’s natural selection can do is kill off the faulty or inferior designs. "

Designs? Whose designs? How did you detect and quantify the design? Why are faulty or inferior designs generated to be killed off?

If you mean selection will act to reduce or eliminate less favored alleles, you are correct. Evolution!

"—it does not induce helpful mutations to magically arise. All evolutionary creations must arise from those random mutations."

Yep. Who has claimed otherwise?

So what we're left with is Cornelius's personal disbelief that random genetic variation plus natural selection is sufficient. There is no data, no empiricism, just his hunch. Random mutations are observed. Less favorable alleles are selected against. How then, is the converse-that more favorable alleles will be selected for even deniable?

And his hunch has been disproved by experiments showing random variation plus selection generates products with novel functions, and by direct observation of evolution in progress.

Randomly hitting the genome at random positions with measurable frequency sounds like a beautifuly designed mechanism. Would you take that farther and by implying that this mechanism in itself came about randomly?

you can trace bacteria evolving through time?
. To the disbelieving shock of many scientists, both ancient and modern bacteria were found to have the almost same exact DNA sequence.

The Paradox of the "Ancient" Bacterium Which Contains "Modern" Protein-Coding Genes:
“Almost without exception, bacteria isolated from ancient material have proven to closely resemble modern bacteria at both morphological and molecular levels.” Heather Maughan*, C. William Birky Jr., Wayne L. Nicholson, William D. Rosenzweig§ and Russell H. Vreeland
http://mbe.oxfordjournals.org/cgi/content/full/19/9/1637

Evolutionists were so disbelieving at this stunning lack of change that they insisted the stunning similarity was due to modern contamination. Yet the following study laid that objection to rest by verifying Dr. Vreeland's methodology was not introducing contamination:

World’s Oldest Known DNA Discovered (419 million years old) - Dec. 2009
Excerpt: But the DNA was so similar to that of modern microbes that many scientists believed the samples had been contaminated. Not so this time around. A team of researchers led by Jong Soo Park of Dalhousie University in Halifax, Canada, found six segments of identical DNA that have never been seen before by science. “We went back and collected DNA sequences from all known halophilic bacteria and compared them to what we had,” Russell Vreeland of West Chester University in Pennsylvania said. “These six pieces were unique.
http://news.discovery.com/earth/oldest-dna-bacteria-discovered.html

These following studies by Dr. Cano preceded Vreeland's work:

“Raul J. Cano and Monica K. Borucki discovered the bacteria preserved within the abdomens of insects encased in pieces of amber. In the last 4 years, they have revived more than 1,000 types of bacteria and microorganisms — some dating back as far as 135 million years ago, during the age of the dinosaurs. In October 2000, another research group used many of the techniques developed by Cano’s lab to revive 250-million-year-old bacteria from spores trapped in salt crystals. With this additional evidence, it now seems that the “impossible” is true.”
http://www.physicsforums.com/showthread.php?t=281961


Revival and identification of bacterial spores in 25- to 40-million-year-old Dominican amber
Dr. Cano and his former graduate student Dr. Monica K. Borucki said that they had found slight but significant differences between the DNA of the ancient, 25-40 million year old amber-sealed Bacillus sphaericus and that of its modern counterpart,(thus ruling out that it is a modern contaminant, yet at the same time confounding materialists, since the change is not nearly as great as evolution's "genetic drift" theory requires.)
http://www.sciencemag.org/cgi/content/abstract/268/5213/1060

30-Million-Year Sleep: Germ Is Declared Alive
http://query.nytimes.com/gst/fullpage.html?res=990CEFD61439F93AA25756C0A963958260&sec=&spon=&pagewanted=2

Dr. Cano's work on ancient bacteria came in for intense scrutiny since it did not conform to Darwinian predictions. Yet Dr. Cano has been vindicated:

“After the onslaught of publicity and worldwide attention (and scrutiny) after the publication of our discovery in Science, there have been, as expected, a considerable number of challenges to our claims, but in this case, the scientific method has smiled on us. There have been at least three independent verifications of the isolation of a living microorganism from amber."
http://www.uncommondescent.com/intelligent-design/reductionist-predictions-always-fail/comment-page-3/#comment-357693

In reply to a personal e-mail from myself, Dr. Cano commented on the "Fitness Test" I had asked him about:
Dr. Cano stated: "We performed such a test, a long time ago, using a panel of substrates (the old gram positive biolog panel) on B. sphaericus. From the results we surmised that the putative "ancient" B. sphaericus isolate was capable of utilizing a broader scope of substrates. Additionally, we looked at the fatty acid profile and here, again, the profiles were similar but more diverse in the amber isolate.":
Fitness test which compared ancient bacteria to its modern day descendants, RJ Cano and MK Borucki

Thus, the most solid evidence available for the most ancient DNA scientists are able to find does not support evolution happening on the molecular level of bacteria. In fact, according to the fitness test of Dr. Cano, the change witnessed in bacteria conforms to the exact opposite, Genetic Entropy a loss of functional information/complexity, since fewer substrates and fatty acids are utilized by the modern strains. Considering the intricate level of protein machinery it takes to utilize individual molecules within a substrate, we are talking an impressive loss of protein complexity, and thus loss of functional information, from the ancient amber sealed bacteria.

I have no idea what the context was. The speaker said he was putting forth a case for discussion. I'm not paying $20 to the creationists who secretly taped him, and decided to turn a profit, to find out.

All I have is his own words, that "In short the article does not fairly represent my views."

"I do not support the creationist movement in any way."

And last, most significantly for you:

"The issue should be resolved by rational discussion, and not by quoting authorities,' which seems to be the creationists' principal mode of argument."

You still haven't apologized for the outrageous and fabricated quotemines you were tossing around previously.

"Randomly hitting the genome at random positions with measurable frequency sounds like a beautifuly designed mechanism."

There's no actual mechanism-these are accidents, induced by UV, chemicals, oxidation, miscopying.

And this "beautiful mechanism" plagues us.
Cancer much?

Although I appreciate science, it's ability to completely suck the grandure and beauty out of life is astonishing. Thank you for making your point so very very clear.

UV + chemicals + oxidation + miscopying = You. an accident.

And how can you not call that a mechanism? A biological explanation of how a feature is created is EXACTLY that. a mechanism. Whatever. You can have the word. It's just a word.

To say that this non-mechanism 'plagues us' seems narrow-minded considering it's your entire explanation for all existence of life (including your own).

Try thinking abstractly for a second. A + B + C + D + Accidents = Life As We Know it. Just because accidents are part of the equation, it doesn't mean that the global function of that equation is an accident. Take B or C out, and you're up the creek. Thank God for B & C!!

Mechanism, process, whatever. My point is that it isn't a single process that has any recognizable feature of design-and has extremely unfortunate effects like cancer.

"Just because accidents are part of the equation, it doesn't mean that the global function of that equation is an accident."

I think you've basically summed up theistic evolution. Maybe one could believe life is intelligently designed to evolve. It would then be the burden of ID to show how that belief could ever translate into science, and why we would dispense with theism-neutral scientific evolution.

I feel you have just proved my original assertion. The term 'random', although it's roots describe the actual process of mutations, the implied dogma is that it's all an accident.

I think that the 'burden' lies more with Evolutionists. Proving the existence of God with Science is a silly notion. Science requires that you measure test and prove it. Since science is the Evolutionists god (cheesy I know), then you have to use science to disprove. i.e. conclude that life exists completely on its own. You don't have bio-genesis yet. You've got some work to do.

"The term 'random', although it's roots describe the actual process of mutations, the implied dogma is that it's all an accident."

So we can't use an accurate term to describe the science, because you mistake it for a dogmatic take on the meaning of life? Wow.

"Since science is the Evolutionists god (cheesy I know), then you have to use science to disprove. i.e. conclude that life exists completely on its own. "

You seem to think it is the goal of science to disprove god? This is silly. Many evolutionists are religious, and many religious people accept evolution. God might end up seeming somewhat superfluous as science's investigation into nature proceeds, but that is religion's problem, and not science's.

Robert C. lets see you are promoting a theory that only survives by the sheer deceptiveness of its adherents and you want me to apologize. You have got to be kidding. Robert I have been called just about every name in the book by neo-Darwinists, have even been threatened with death by a couple of times, Yet I have never even seen so much as a sniffle of remorse from any of your comrades,, As well, I have consistently presented evidence that shows evolution to be false, yet neo-Darwinists never even engage the evidence when it gets hot and heavy, they just hide in obfuscation or play meaningless games as you are doing right now. As far as I can It never is about the evidence with neo-Darwinists but always about protecting their atheistic religion no matter what lie they have to tell.

ba77 wrote:
"As well, I have consistently presented evidence that shows evolution to be false,…"

You've cut and pasted quotes. The evidence is in the figures and tables of the primary literature, but you don't even look at those.

". yet neo-Darwinists never even engage the evidence when it gets hot and heavy, they just hide in obfuscation or play meaningless games as you are doing right now."

Who produces the evidence, ba? Our side or yours?

"As far as I can It never is about the evidence with neo-Darwinists but always about protecting their atheistic religion no matter what lie they have to tell."

Yet the neo-Darwinists produce the evidence, while your side produces nothing but rhetoric. Project much?

Smokey states:
"You've cut and pasted quotes. The evidence is in the figures and tables of the primary literature, but you don't even look at those."

"Who produces the evidence, ba? Our side or yours?"

I didn't know truth had a side

"Yet the neo-Darwinists produce the evidence, while your side produces nothing but rhetoric. Project much?"

Wrong, neo-Darwinists force feed the evidence into their twisted atheistic worldview which in due time will be taught in history classes as a prime example of propaganda driven science. i.e. rhetoric!

here are some more quotes for you to deny the validity of:

“But in all the reading I’ve done in the life-sciences literature, I’ve never found a mutation that added information… All point mutations that have been studied on the molecular level turn out to reduce the genetic information and not increase it.”
Lee Spetner - Ph.D. Physics - MIT - Not By Chance

"Bergman (2004) has studied the topic of beneficial mutations. Among other things, he did a simple literature search via Biological Abstracts and Medline. He found 453,732 “mutation” hits, but among these only 186 mentioned the word “beneficial” (about 4 in 10,000). When those 186 references were reviewed, almost all the presumed “beneficial mutations” were only beneficial in a very narrow sense- but each mutation consistently involved loss of function changes-hence loss of information.” Sanford: Genetic Entropy

“Mutations, in summary, tend to induce sickness, death, or deficiencies. No evidence in the vast literature of heredity change shows unambiguous evidence that random mutation itself, even with geographical isolation of populations leads to speciation.”
Lynn Margulis - Acquiring Genomes [2003], p. 29.

Estimation of spontaneous genome-wide mutation rate parameters: whither beneficial mutations? (Thomas Bataillon)
Abstract. It is argued that, although most if not all mutations detected in mutation accumulation experiments are deleterious, the question of the rate of favourable mutations (and their effects) is still a matter for debate.
http://www.nature.com/hdy/journal/v84/n5/full/6887270a.htm

Neo-darwinian-driven science is IDs best friend. Keep peeling and you'll keep finding layer after layer of embedded information and intelligence-mechanisms. It can be fruitful science, even if it is wrong in its underlying assumptions.

Not being a biologist, I thought it would be instructive (for me) to evaluate one of your references a little. Taking:

“Mutations, in summary, tend to induce sickness, death, or deficiencies. No evidence in the vast literature of heredity change shows unambiguous evidence that random mutation itself, even with geographical isolation of populations leads to speciation.”
Lynn Margulis - Acquiring Genomes [2003], p. 29.

I found the book and the following description:

How do new species evolve? Although Darwin identified inherited variation as the creative force in evolution, he never formally speculated where it comes from. His successors thought that new species arise from the gradual accumulation of random mutations of DNA. But despite its acceptance in every major textbook, there is no documented instance of it. Lynn Margulis and Dorion Sagan take a radically new approach to this question. They show that speciation events are not, in fact, rare or hard to observe. Genomes are acquired by infection, by feeding, and by other ecological associations, and then inherited. Acquiring Genomes is the first work to integrate and analyze the overwhelming mass of evidence for the role of bacterial and other symbioses in the creation of plant and animal diversity. It provides the most powerful explanation of speciation yet given.

I see nothing here supporting ID. In fact, phrases like "They show that speciation events are not, in fact, rare or hard to observe." directly oppose the ID view that speciation requires special assistance from a designer. The last sentence "It provides the most powerful explanation of speciation yet given" is a direct challenge to ID.

Further reading on Margulis includes descriptions of how her work has become a cornerstone of evolutionary theory.

And yet you provide this to support your position? Very odd.

Let's take Margulis's symbiotic speciation one step further, since symbiosis was "speculative" in the first place so as to replace the complete failure of random mutations to produce information, (why does the failure of random mutations to produce information not interest you?) and Let's just see what the actual empirical evidence says about symbiosis at the most basic level Mike:

Bacteria Too Complex To Be Primitive Eukaryote Ancestors - July 2010
Excerpt: “Bacteria have long been considered simple relatives of eukaryotes,” wrote Alan Wolfe for his colleagues at Loyola. “Obviously, this misperception must be modified. There is a whole process going on that we have been blind to.”. For one thing, Forterre and Gribaldo revealed serious shortcomings with the popular “endosymbiosis” model – the idea that a prokaryote engulfed an archaea and gave rise to a symbiotic relationship that produced a eukaryote.
http://www.creationsafaris.com/crev201007.htm#20100712b

Thus Mike, I will take her observations on random mutations and call her bluff on symbiosis!

Thus Mike, I will take her observations on random mutations and call her bluff on symbiosis!

Ok. So let's say you are correct and Margulis is wrong. How does this say anything about ID?

There is a certain amount of irony in this discussion. In many respects, ID has a symbiotic relationship with evolution - without any direct evidence of a designer, ID is forced to depend on finding weaknesses in evolution to advance its case. While a gap in our understanding of evolution says little or nothing about the validity of ID, it can be made to appear that way this is primarily due to the success of evolution in absorbing or superseding other naturalistic explanations so that no other naturalistic options seem plausible.

In that sense, ID has something of a parasitic relationship with evolution - it depends on the strength of that which it wishes to destroy.

The primary strengh of ID, IMHO, is the fact that organism look like they were designed. If I compare a cell to something I know was nit designed, like a rock, and something that was designed, like a car, the cell looks more like the thing that was designed.

ID has a symbiotic relationship with evolution - without any direct evidence of a designer,

well I beg to differ. if anything has a symbiotic relationship with anything else in this deal, evolution is parasitic dependence on Theism and the ordered structure of science that the Theistic philosophy itself has founded! As well, the actions of Quantum Mechanics, which blatantly defy our concepts of time and space, gives direct evidence of a cause which is completely transcendent of time and space and thus completely undermines the materialistic presupposition of a "local reality" upon which evolution is built. Thus in complete truth of the matter, evolution has no direct evidence for the material entity that it presupposes to be the basis of its reality whereas Theism does have direct evidence of a transcendent cause for reality! As well as Dr. Hunter repeatedly points out evolutionists continually ignore overwhelming evidence for design by appealing to Theistic arguments. i.e. they say "God would not have done such and such that way". So Mike tell me exactly how evolution is not being parasitic in its form of argumentation here?

They're called quote-mines, because when you took the quote out of context, you changed the author's intended meaning.

An appeal to authority is valid when

* The cited authority has sufficient expertise.
* The authority is making a statement within their area of expertise.
* The area of expertise is a valid field of study.
* There is adequate consensus among authorities in the field and the authority is presenting that consensus.
* There is no evidence of undue bias.
(The proper argument against a valid appeal to authority is to the evidence.)

Your cite to authority failed because you simply haven't properly represented the views of the scientists you quoted, that the consensus view is, from your omission, "speciation events are not, in fact, rare or hard to observe."

bornagain77: As well, the actions of Quantum Mechanics, which blatantly defy our concepts of time and space, gives direct evidence of a cause which is completely transcendent of time and space and thus completely undermines the materialistic presupposition of a "local reality" upon which evolution is built.

We can directly observe many of the mechanisms of evolution and can show that "local realism" is sufficient to explain complex adaptation. We can't show a monolith didn't tamper with the course of hominid evolution, but there is no scientific evidence to support that, or any similar supposition.

bornagain77 wrote: As well, the actions of Quantum Mechanics, which blatantly defy our concepts of time and space, gives direct evidence of a cause which is completely transcendent of time and space and thus completely undermines the materialistic presupposition of a "local reality" upon which evolution is built.

Don't spout nonsense. Quantum mechanics does not defy concepts of space and time. Paradoxes arise from naive attempts to reduce quantum physics to classical concepts. But quantum mechanics respects the fundamental principles of physics like causality, Lorentz invariance and conservation laws.

The bulldozer is a very apt metaphor as you bulldoze through the inane rational for evolution. Nobody does it quite as good as you.

ba77: As well as Dr. Hunter repeatedly points out evolutionists continually ignore overwhelming evidence for design by appealing to Theistic arguments. i.e. they say "God would not have done such and such that way".

This is, of course, a specious argument. If adaptation construed as evidence for conscious "design" is a scientific argument, then the counterargument, citing evidence of poor, clumsy, and nonsensical constructions as evidence that life is not the result of conscious design is also scientific. Hunter and his ilk cannot have it both ways.

John: If adaptation construed as evidence for conscious "design" is a scientific argument, then the counterargument, citing evidence of poor, clumsy, and nonsensical constructions as evidence that life is not the result of conscious design is also scientific.

The scientific argument is that a designer is an extraneous entity for explaining biological patterns such as the nested hierarchy, which have simple and well-tested natural explanations.

ID Proponents are not trying to have it both ways. They address the problems of bad design. It's just that no one can really say just what an omniscient designer would or would not do.

oleg, once again I remind you that perhaps you would like to write Alain Aspect, so as to correct him, since you think you know so much more than he does as to the complete failure of materialism, as it has been classically understood, to explain reality.

The Failure Of Local Realism - Materialism - Alain Aspect - video
http://www.metacafe.com/watch/4744145/

John you say in response to this:

evolutionists argue God would not have done such and such that way".

"This is, of course, a specious argument."

That is very humorous, please come forward with this "truth" of yours the next time a evolutionist tells me that the miracle of my eyesight actually evolved because God would not have designed the inverted retina and not because of any actual observational evidence he can present for eyes evolving.

Retinal Glial Cells Enhance Human Vision Acuity A. M. Labin and E. N. Ribak
Physical Review Letters, 104, 158102 (April 2010)
Excerpt: The retina is revealed as an optimal structure designed for improving the sharpness of images.
http://www.uncommondescent.com/intelligent-design/why-ken-miller-is-right-about-our-backward-retina/#comment-354274

"Evolution" gave flawed eye better vision
Excerpt: IT LOOKS wrong, but the strange, "backwards" structure of the vertebrate retina actually improves vision. . Their findings suggest that sending light via the Müller cells offers several advantages. At least two types of light get inside the eye: light carrying image information, which comes directly through the pupil, and "noise" that has already been reflected multiple times within the eye. The simulations showed that the Müller cells transmit a greater proportion of the former to the rods and cones below, while the latter tends to leak out. This suggests the cells act as light filters, keeping images clear.
http://www.uncommondescent.com/intelligent-design/the-blind-leading-the-blind/#comment-354157

Moreover, the vestigial organ argument, like the "Junk DNA argument, is basically the "Bad Design" argument which is used by evolutionists. A argument that quickly leaves the field of empirical science and enters squarely into the field of Philosophical debate.

Refuting The Myth Of "Bad Design" vs. Intelligent Design - William Lane Craig - video
http://www.youtube.com/watch?v=uIzdieauxZg

The primary strengh of ID, IMHO, is the fact that organism look like they were designed. If I compare a cell to something I know was nit designed, like a rock, and something that was designed, like a car, the cell looks more like the thing that was designed.

That something merely "looks designed" is about a subjective and unscientific way for making your case as can be. Fluffy clouds can sometimes look like cars, houses, etc. but that doesn't make the clouds designed. And suppose what "looks designed" to you doesn't look designed to most everyone else? How do you decide who is right?

Another big problem with your logic is the how superficially the "looks designed" applies. Once you get down to examining the details, cells and cars are nothing at all alike.

What IDCers need to do, and have never done, is to come up with an objective way for determining their claimed designs in living organisms. So they just keep riding the personal incredulity train and wondering why science ignores their fact-free claims.

I have already told you that local realism has nothing to do with philosophy, so don't equate it with materialism. You don't know what you are talking about.

ID Proponents are not trying to have it both ways. They address the problems of bad design. It's just that no one can really say just what an omniscient designer would or would not do.

BINGO! That's why IDC isn't science. ToE explains quite well and gives logical, supported with evidence reasons for why we see the kluged together biological functions we do. The IDC handwave "the Designed works in mysterious ways" explains nothing.

"You don't know what you are talking about."

but of course just dismiss me. I am a ignorant hick bumpkin creationist am I not.

Yet regardless of what you may think of my mental capacity, or lack thereof, or my grasp on QM for that matter, methinks you are much to easily impressed with your own intelligence on the QM matter so as to deceive yourself into thinking Quantum Mechanics does not completely overthrow classical materialistic thought:

Why Quantum Theory Does Not Support Materialism - By Bruce L Gordon:
Excerpt: Because quantum theory is thought to provide the bedrock for our scientific understanding of physical reality, it is to this theory that the materialist inevitably appeals in support of his worldview. But having fled to science in search of a safe haven for his doctrines, the materialist instead finds that quantum theory in fact dissolves and defeats his materialist understanding of the world.
http://www.4truth.net/site/c.hiKXLbPNLrF/b.2904125/k.E94E/Why_Quantum_Theory_Does_Not_Support_Materialism.htm

Wrong, neo-Darwinists force feed the evidence into their twisted atheistic worldview which in due time will be taught in history classes as a prime example of propaganda driven science. i.e. rhetoric!

Ba77, this is an Area 51 argument, dangerously close to conspiracy mongering.

Refuting The Myth Of "Bad Design" vs. Intelligent Design - William Lane Craig - video
http://www.youtube.com/watch?v=uIzdieauxZg

It's fun to josh with creationists. For years the creationists would insist on the miraculousness of some organelle or process, unmindful of the utter uselessness of such posturing, and their lack of scientific merit. When the science advocate turned the tables by pointing out the flaws in certain human structures, the creationists flipped to claim that bad design does not mean absence of design. Enter the likes of preachers like Craig (who have zero scientific credentials, zero scientific accomplishments, and zero scientific capabilities) who find the ground suddenly slipping, and come up with a rejoinder of how the "bad design" actually is "good design"! So then Ba77 what is it? Is it good design or bad design? We know what it is of course, it is no design. Because the term design is not even worthy of being a placeholder, it is an empty and useless term, outside the context of what we use everyday. The design nonsense is not even an invention of the neo-creationists (aka IDs). They plagiarised it (without acknowledgment) from the paleo-creationists.

so ibeck, please tell me exactly how many vestigial organs you still believe in and please tell me exactly what percentage of junk DNA do you still believe in, and please tell me if you still believe the inverted retina to be a prime example of "bad design"

Retinal Glial Cells Enhance Human Vision Acuity A. M. Labin and E. N. Ribak
Physical Review Letters, 104, 158102 (April 2010)
Excerpt: The retina is revealed as an optimal structure designed for improving the sharpness of images.
http://www.uncommondescent.com/intelligent-design/why-ken-miller-is-right-about-our-backward-retina/#comment-354274

"Evolution" gave flawed eye better vision
Excerpt: IT LOOKS wrong, but the strange, "backwards" structure of the vertebrate retina actually improves vision. . Their findings suggest that sending light via the Müller cells offers several advantages. At least two types of light get inside the eye: light carrying image information, which comes directly through the pupil, and "noise" that has already been reflected multiple times within the eye. The simulations showed that the Müller cells transmit a greater proportion of the former to the rods and cones below, while the latter tends to leak out. This suggests the cells act as light filters, keeping images clear.
http://www.uncommondescent.com/intelligent-design/the-blind-leading-the-blind/#comment-354157

ibeck let me show you a "area 51" argument:

Richard Dawkins Vs. Ben Stein - The UFO Interview - video
http://www.metacafe.com/watch/4134259

Bruce Gordon goes off the rails when he writes this: When such local variables are introduced, the predictions of the modified theory differ from those of quantum mechanics. A series of experiments beginning with those conducted by Alain Aspect at the University of Paris in the 1980s has demonstrated quite conclusively that quantum theory, not some theory modified by local hidden parameters, generates the correct predictions. The physical world, therefore, is fundamentally nonlocal and permeated with instantaneous connections and correlations.

That simply does not follow. Quantum mechanics is an explicitly local theory. It's attempts to reduce it to classical physics that make it nonlocal. Don't try to square the circle and everything will be all right. Quantum mechanics is not reducible to classical. The physical world exhibits locality and causality, it's just not classical.

bornagain77: many vestigial organs you still believe in

Vestigiality doesn't mean the structure doesn't have a function.

The bulldozer is a very apt metaphor as you bulldoze through the inane rational for evolution. Nobody does it quite as good as you.

You got the 'bull' part right anyway.

so ibeck, please tell me exactly how many vestigial organs you still believe in

BA77, what does the word vestigial mean to you?

"You got the 'bull' part right anyway. "

That's hilarious considering the extreme claim of evolution to explain all biological life in contrast to the complete lack of scientific proof.
.

oleg, since finite "local" reality in fact arises from the infinite non-local world of QM, as is clearly demonstrated by Aspect though you refuse to see it, your attempts to separate the two worlds just so as to preserve your "local" thinking of materialism is vain. And I might add you unreasonableness is another shining example of materialistic thought impeding true scientific progress, at least for those who dogmatically cling to a materialistic/atheistic worldview in spite of the evidence screaming otherwise.

The Mental Universe - Richard Conn Henry - Professor of Physics John Hopkins University
Excerpt: The only reality is mind and observations, but observations are not of things. To see the Universe as it really is, we must abandon our tendency to conceptualize observations as things. The Universe is immaterial — mental and spiritual. Live, and enjoy.

"As a man who has devoted his whole life to the most clear headed science, to the study of matter, I can tell you as a result of my research about atoms this much: There is no matter as such. All matter originates and exists only by virtue of a force which brings the particle of an atom to vibration and holds this most minute solar system of the atom together. We must assume behind this force the existence of a conscious and intelligent mind. This mind is the matrix of all matter."
Max Planck - The Father Of Quantum Mechanics - (Of Note: Planck was a devout Christian, which is not surprising when you realize practically every founder of each major branch of modern science also had a deep Christian connection.)

Like junk DNA of today for many years materialists predicted much of human anatomy was vestigial. Yet once again, they were proven completely wrong in this prediction.

“The thyroid gland, pituitary gland, thymus, pineal gland, and coccyx, … once considered useless by evolutionists, are now known to have important functions. The list of 180 “vestigial” structures is practically down to zero. Unfortunately, earlier Darwinists assumed that if they were ignorant of an organ’s function, then it had no function.” "Tornado in a Junkyard" - book - by former atheist James Perloff

For a prime example of evolution's failed predictions of vestigial organs, recently in October 2007, the appendix has been found to have essential purpose in the human body:

Appendix has purpose:
Excerpt: "The appendix acts as a good safe house for bacteria," said Duke surgery professor Bill Parker.
http://en.wikinews.org/wiki/Scientists:_appendix_has_purpose

"You got the 'bull' part right anyway. "

That's hilarious considering the extreme claim of evolution to explain all biological life in contrast to the complete lack of scientific proof.

LOL! Science doesn't provide proof. Science provides evidence.

There are thousand of colleges, universities, libraries, natural history museums, genetic laboratories, biotech companies, etc. in the world where the evidence may be seen. There are hundreds of peer reviewed scientific journals publishing newly discovered evidence every day. There are any number of good sites on line like here where you can get an overview of this evidence, or you could study the primary scientific literature directly. But you'll never cure your willful ignorance until you decide to look and learn.

ba77 wrote: oleg, since finite "local" reality in fact arises from the infinite non-local world of QM, as is clearly demonstrated by Aspect though you refuse to see it

This is gibberish. Don't tell me what Aspect has done, I know that well enough. Learn some quantum mechanics yourself. (I'm not holding my breath.)

For a prime example of evolution's failed predictions of vestigial organs, recently in October 2007, the appendix has been found to have essential purpose in the human body:

Hey BA77, vestigial doesn't mean "has no purpose". Vestigial means having lost or been modified from its original function.

When you IDiots can't even get the simple scientific meaning of a term right, why are you surprised that science doesn't take your critiques seriously?

Andreas: If Penicillin is present in the environment, those individuals that are resistant are much more likely to reproduce than the individuals that are not resistant - which causes the allele(s) mediating resistance to penicillin to spread in the population. Whether you call this process an "active force" (how would you define this term ?) or not is mere semantics.

I am not quite sure what to make of bacteria developing resistance to penicillin. The fact that such experiments end up with the same results time after time suggests something more than true randomness.

In this case, the term "selection pressure" (maybe "selection factor" is a better term) is in a loose sense applicable. There appears to be a cause and effect relationship.

What about macroevolutionary events or seqeunces? What are the environmental pressures or factors that cause the major morphological trasformations evidenced in the evolution of the whale for example?

If you could run a multi-million year experiment, what environmental variables would you change to effect the land mammal to whale tranformation? This would be like a giant anti-bacterial resistance experiment. Or would it?

If Gould is correct (if you replayed the tape of history. ), your hypothetical experiment would not have the same outcome as what is observed in the fossil record.

About the only thing such an experiment would demonstrate is the mutations, indeed, do not "magically arise."

ibeck let me show you a "area 51" argument:
Richard Dawkins Vs. Ben Stein - The UFO Interview - video http://www.metacafe.com/watch/4134259

Richard doesn't debate creationists and quacks, so that's not Ben Whine debating Dawkins. It is simply a cut-and-paste. If you want to debate Dawkins present yourself at one of his lectures and talk to him. Don't use cat's paws like Ben Whine.

Dr.Henry or for that matter Dr. Planck's assertions are only as valid as their evidence. In neither case have they offered any evidence for mind/consciousness etc., not even some pseudomathematical "proof" (obviously they valued their discipline far, far, higher than did Swell). And besides Planck was simply channeling a Cliff Notes version of Advaita Vedanta which was popular in Germany for over a 100 years by Planck's time.

And since this is quote time, some quotes from Einstein

To assume the existence of an unperceivable being . does not facilitate understanding the orderliness we find in the perceivable world.
I don't try to imagine a God it suffices to stand in awe of the structure of the world, insofar as it allows our inadequate senses to appreciate it. I have never imputed to Nature a purpose or a goal, or anything that could be understood as anthropomorphic. What I see in Nature is a magnificent structure that we can comprehend only very imperfectly, and that must fill a thinking person with a feeling of humility. This is a genuinely religious feeling that has nothing to do with mysticism. A man's moral worth is not measured by what his religious beliefs are but rather by what emotional impulses he has received from Nature during his lifetime. My religion consists of a humble admiration of the illimitable superior spirit who reveals himself in the slight details we are able to perceive With our frail and feeble minds. That deeply emotional conviction of the presence of a superior reasoning power, which is revealed in the incomprehensible Universe, forms my idea of God

And yet, though Einstein was overturned in his materialistic based steady state postulation for the age of the universe, and his hidden variable postulation for quantum mechanics, you are going to trust his "intuitions" over the evidence? How special to look so blindly at what you only want to see. Myself I call that denialism.

oleg, though Aspect is crystal clear that local realism is falsified, you deny this and pretend that you know better. In fact you state completely contrary to Aspect:

"Quantum mechanics is an explicitly local theory."

What's more you consider yourself so much wiser than anything anyone else says contrary to your "local" materialistic worldview that you consider them ignorant, no matter what position they hold, and yourself superior. Go on with your fantasies if it comforts you, but don't expect me to join you in your delusions!

Thorton, since you think vestigial has always meant "having partial function" why don't you go back and erase all those needless tonsil, tailbone, appendix, etc.. etc.. removals that mutilated millions

ba77 wrote: leg, though Aspect is crystal clear that local realism is falsified, you deny this and pretend that you know better. In fact you state completely contrary to Aspect:

ba, you can't even comprehend what I am saying. Of course local realism has been falsified. It's a specific set of ideas that is different from locality principles obeyed by the quantum field theory (the relativistic version of quantum mechanics). Local realism tries to blame quantum indeterminacy on the existence of local classical variables. That has been disproved. Locality of QFT remains valid.

"Of course local realism has been falsified."

thus oleg materialism, as it has been classically defined to an "atom" through the centuries, is falsified.

Materialism has had to undergo dramatic revision to account for this . MWI, yet evolutionists act as if they are dealing strictly with Newtonian physics, save for Koonin here:

I like this following paper for though it is materialistic in its outlook at least Eugene Koonin, unlike many materialists, is brutally honest with the evidence we now have.

The Biological Big Bang model for the major transitions in evolution - Eugene V Koonin - Background:
"Major transitions in biological evolution show the same pattern of sudden emergence of diverse forms at a new level of complexity. The relationships between major groups within an emergent new class of biological entities are hard to decipher and do not seem to fit the tree pattern that, following Darwin's original proposal, remains the dominant description of biological evolution. The cases in point include the origin of complex RNA molecules and protein folds major groups of viruses archaea and bacteria, and the principal lineages within each of these prokaryotic domains eukaryotic supergroups and animal phyla. In each of these pivotal nexuses in life's history, the principal "types" seem to appear rapidly and fully equipped with the signature features of the respective new level of biological organization. No intermediate "grades" or intermediate forms between different types are detectable
http://www.biology-direct.com/content/2/1/21

Biological Big Bangs - Origin Of Life and Cambrian - Dr. Fazale Rana - video
http://www.metacafe.com/watch/4284466

It should be noted that Koonin tries to account for the origination of the massive amounts of functional information, required for the Cambrian Explosion, and other “explosions”, by trying to access an “unelucidated and undirected” mechanism of Quantum Mechanics called ‘Many Worlds’. Besides Koonin ignoring the fact that Quantum Events, on a whole, are strictly restricted to the transcendent universal laws/constants of the universe, including, and especially, the second law of thermodynamics, for as far back in time in the universe as we can see, it is also fair to note, in criticism to Koonin’s scenario, that appealing to the undirected infinite probabilistic resource, of the quantum mechanics of the Many Worlds scenario, actually greatly increases the amount of totally chaotic information one would expect to see generated “randomly” in the fossil record. In fact the Many Worlds scenario actually greatly increases the likelihood we would witness total chaos surrounding us:


Problem 3: Step-by-Step Random Mutations Cannot Generate the Genetic Information Needed for Irreducible Complexity

Editor’s note: This is Part 3 of a 10-part series based upon Casey Luskin’s chapter, “The Top Ten Scientific Problems with Biological and Chemical Evolution,” in the volume More than Myth, edited by Paul Brown and Robert Stackpole (Chartwell Press, 2014). The full chapter can be found online here. Other individual installments can be found here: Problem 1, Problem 2, Problem 4, Problem 5, Problem 6, Problem 7, Problem 8, Problem 9, Problem 10.

According to evolutionary biologists, once life got started, Darwinian evolution took over and eventually produced the grand diversity we observe today. Under the standard view, a process of random mutation and natural selection built life’s vast complexity one small mutational step at a time. All of life’s complex features, of course, are thought to be encoded in the DNA of living organisms. Building new features thus requires generating new information in the genetic code of DNA. Can the necessary information be generated in the undirected, step-by-step manner required by Darwin’s theory?

Most everyone agrees that Darwinian evolution tends to work well when each small step along an evolutionary pathway provides some survival advantage. Darwin-critic Michael Behe notes that “if only one mutation is needed to confer some ability then Darwinian evolution has little problem finding it.” 24 However, when multiple mutations must be present simultaneously to gain a functional advantage, Darwinian evolution gets stuck. As Behe explains, “If more than one [mutation] is needed, the probability of getting all the right ones grows exponentially worse.” 25

Behe, a professor of biochemistry at Lehigh University, coined the term “irreducible complexity” to describe systems which require many parts — and thus many mutations — to be present — all at once — before providing any survival advantage to the organism. According to Behe, such systems cannot evolve in the step-by-step fashion required by Darwinian evolution. As a result, he maintains that random mutation and unguided natural selection cannot generate the genetic information required to produce irreducibly complex structures. Too many simultaneous mutations would be required — an event which is highly unlikely to occur.

Observation of this problem is not limited to Darwin-critics. A paper by a prominent evolutionary biologist in the prestigious journal Proceedings of the U.S. National Academy of Science. acknowledges that “simultaneous emergence of all components of a system is implausible.” 26 Likewise, University of Chicago evolutionary biologist Jerry Coyne — a staunch defender of Darwinism — admits that “natural selection cannot build any feature in which intermediate steps do not confer a net benefit on the organism.” 27 Even Darwin intuitively recognized this problem, as he wrote in Origin of Species:

If it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. 28

Evolutionary scientists like Darwin and Coyne claim they know of no real-world case where Darwinian selection gets blocked in this manner. But they would agree, at least in principle, that there are theoretical limits to what Darwinian evolution can accomplish: If a feature cannot be built by “numerous, successive, slight modifications,” and if “intermediate steps do not confer a net benefit on the organism,” then Darwinian evolution will “absolutely break down.”

The problems are real. Modern biology continues to uncover more and more examples where biological complexity seems to outstrip the information-generative capacity of Darwinian evolution.

Molecular Machines
In his book Darwin’s Black Box, Michael Behe discusses molecular machines which require multiple parts to be present before they could function and confer any advantage on the organism. Behe’s most famous example is the bacterial flagellum — a micromolecular rotary-engine, functioning like an outboard motor on bacteria to propel it through liquid medium to find food. In this regard, flagella have a basic design that is highly similar to some motors made by humans containing many parts that are familiar to engineers, including a rotor, a stator, a u-joint, a propeller, a brake, and a clutch. As one molecular biologist writes in the journal Cell, “[m]ore so than other motors, the flagellum resembles a machine designed by a human.” 29 However the energetic efficiency of these machines outperforms anything produced by humans: the same paper found that the efficiency of the bacterial flagellum “could be

There are various types of flagella, but all use certain basic components. As one paper in Nature Reviews Microbiology acknowledges, “all (bacterial) flagella share a conserved core set of proteins” since “Three modular molecular devices are at the heart of the bacterial flagellum: the rotor-stator that powers flagellar rotation, the chemotaxis apparatus that mediates changes in the direction of motion and the T3SS that mediates export of the axial components of the flagellum.” 31 As this might suggest, the flagellum is irreducibly complex. Genetic knockout experiments have shown that it fails to assemble or function properly if any one of its approximately 35 genes are missing. 32 In this all-or-nothing game, mutations cannot produce the complexity needed to provide a functional flagellar rotary engine one incremental step at a time, and the odds are too daunting for it to assemble in one great leap. Indeed, the aforementioned Nature Reviews Microbiology paper admitted that “the flagellar research community has scarcely begun to consider how these systems have evolved.” 33

Yet the flagellum is just one example of thousands of known molecular machines in biology. One individual research project reported the discovery of over 250 new molecular machines in yeast alone. 34 The former president of the U.S. National Academy of Sciences, Bruce Alberts, wrote an article in the journal Cell praising the “speed,” “elegance,” “sophistication,” and “highly organized activity” of these “remarkable” and “marvelous” molecular machines. He explained what inspired those words: “Why do we call the large protein assemblies that underlie cell function protein machines? Precisely because, like machines invented by humans to deal efficiently with the macroscopic world, these protein assemblies contain highly coordinated moving parts.” 35 Biochemists like Behe and others believe that with all of their coordinated interacting parts, many of these machines could not have evolved in a step-by-step Darwinian fashion.

But it’s not just multi-part machines which are beyond reach of Darwinian evolution. The protein-parts themselves which build these machines would also require multiple simultaneous mutations in order to arise.

Research Challenges the Darwinian Mechanism
In 2000 and 2004, protein scientist Douglas Axe published experimental research in the Journal of Molecular Biology on mutational sensitivity tests he performed on enzymes in bacteria. 36 Enzymes are long chains of amino acids which fold into a specific, stable, three-dimensional shape in order to function. Mutational sensitivity experiments begin by mutating the amino acid sequences of those proteins, and then testing the mutant proteins to determine whether they can still fold into a stable shape, and function properly. Axe’s research found that amino acid sequences which yield stable, functional protein folds may be as rare as 1 in 10 74 sequences, suggesting that the vast majority of amino acid sequences will not produce stable proteins, and thus could not function in living organisms.

Because of this extreme rarity of functional protein sequences, it would be very difficult for random mutations to take a protein with one type of fold, and evolve it into another, without going through some non-functional stage. Rather than evolving by “numerous, successive, slight modifications,” many changes would need to occur simultaneously to “find” the rare and unlikely amino acid sequences that yield functional proteins. To put the matter in perspective, Axe’s results suggest that the odds of blind and unguided Darwinian processes producing a functional protein fold are less than the odds of someone closing his eyes and firing an arrow into the Milky Way galaxy, and hitting one pre-selected atom. 37

Proteins commonly interact with other molecules through a “hand-in-glove” fit, but these interactions often require multiple amino acids to be ‘just right’ before they occur. In 2004, Behe, along with University of Pittsburgh physicist David Snoke, simulated the Darwinian evolution of such protein-protein interactions. Behe and Snoke’s calculations found that for multicellular organisms, evolving a simple protein-protein interaction which required two or more mutations in order to function would probably require more organisms and generations than would be available over the entire history of the Earth. They concluded that “the mechanism of gene duplication and point mutation alone would be ineffective…because few multicellular species reach the required population sizes.” 38

Four years later during an attempt to refute Behe’s arguments, Cornell biologists Rick Durrett and Deena Schmidt ended up begrudgingly confirming he was basically correct. After calculating the likelihood of two simultaneous mutations arising via Darwinian evolution in a population of humans, they found that such an event “would take > 100 million years.” Given that humans diverged from their supposed common ancestor with chimpanzees only 6 million years ago, they granted that such mutational events are “very unlikely to occur on a reasonable timescale.” 39

Now a defender of Darwinism might reply that these calculations measured the power of the Darwinian mechanism only within multicellular organisms where it is less efficient because these more complex organisms have smaller population sizes and longer generation times than single-celled prokaryotic organisms like bacteria. Darwinian evolution, the Darwinian notes, might have a better shot when operating in organisms like bacteria, which reproduce more rapidly and have much larger population sizes. Scientists skeptical of Darwinian evolution are aware of this objection, and have found that even within more-quickly evolving organisms like bacteria, Darwinian evolution faces great limits.

In 2010, Douglas Axe published evidence indicating that despite high mutation rates and generous assumptions favoring a Darwinian process, molecular adaptations requiring more than six mutations before yielding any advantage would be extremely unlikely to arise in the history of the Earth.

The following year, Axe published research with developmental biologist Ann Gauger regarding experiments to convert one bacterial enzyme into another closely related enzyme — the kind of conversion that evolutionists claim can easily happen. For this case they found that the conversion would require a minimum of at least seven simultaneous changes, 40 exceeding the six-mutation-limit which Axe had previously established as a boundary of what Darwinian evolution is likely to accomplish in bacteria. Because this conversion is thought to be relatively simple, it suggests that more complex biological features would require more than six simultaneous mutations to give some new functional advantage.

In other experiments led by Gauger and biologist Ralph Seelke of the University of Wisconsin, Superior, their research team broke a gene in the bacterium E. coli required for synthesizing the amino acid tryptophan. When the bacteria’s genome was broken in just one place, random mutations were capable of “fixing” the gene. But even when only two mutations were required to restore function, Darwinian evolutionseemed to get stuck, with an inability to regain full function. 41

These kind of results consistently suggest that the information required for proteins and enzymes to function is too great to be generated by Darwinian processes on any reasonable evolutionary timescale.

Darwin Skeptics Abound
Drs. Axe, Gauger, and Seelke are by no means the only scientists to observe the rarity of amino acid sequences that yield functional proteins. A leading college-level biology textbook states that “even a slight change in primary structure can affect a protein’s conformation and ability to function.” 42 Likewise, evolutionary biologist David S. Goodsell writes:

[O]nly a small fraction of the possible combinations of amino acids will fold spontaneously into a stable structure. If you make a protein with a random sequence of amino acids, chances are that it will only form a gooey tangle when placed in water. 43

Goodsell goes on to assert that “cells have perfected the sequences of amino acids over many years of evolutionary selection.” But if functional protein sequences are rare, then it is likely that natural selection will be unable to take proteins from one functional genetic sequence to another without getting stuck in some maladaptive or non-beneficial intermediate stage.

The late biologist Lynn Margulis, a well-respected member of the National Academy of Sciences until her death in 2011, once said “new mutations don’t create new species they create offspring that are impaired.” 44 She further explained in a 2011 interview:

[N]eo-Darwinists say that new species emerge when mutations occur and modify an organism. I was taught over and over again that the accumulation of random mutations led to evolutionary change-led to new species. I believed it until I looked for evidence. 45

Similarly, past president of the French Academy of Sciences, Pierre-Paul Grasse, contended that “[m]utations have a very limited ‘constructive capacity'” because “[n]o matter how numerous they may be, mutations do not produce any kind of evolution.” 46


Mutation and the evolution of ageing: from biometrics to system genetics

A notable success for evolutionary genetics during the past century was to generate a coherent, quantitative explanation for an apparent evolutionary paradox: the tendency for multicellular organisms to show declining fitness with age (senescence, often referred to simply as ‘ageing’). This general theory is now widely accepted and explains most of the features of senescence that are observed in natural and laboratory populations, but specific instantiations of that theory have been more controversial. To date, most of the empirical tests of these models have relied on data generated from biometric experiments. Modern population genetics and genomics provide new, and probably more powerful, ways to test ideas that are still controversial more than half a century after the original theory was developed. System-genetic experiments have the potential to address both evolutionary and mechanistic questions about ageing by identifying causal loci and the genetic networks with which they interact. Both the biometrical approaches and the newer approaches are reviewed here, with an emphasis on the challenges and limitations that each method faces.

References

2009 Systems genetics of complex traits in Drosophila melanogaster . Nat. Genet. 41, 299–307. (doi:10.1038/ng.332). Crossref, PubMed, ISI, Google Scholar

. 2005 Hamilton's indicators of the force of selection . Proc. Natl Acad. Sci. USA 102, 8263–8268. (doi:10.1073/pnas.0502155102). Crossref, PubMed, Google Scholar

Benfey P. N.& Mitchell-Olds T.

. 2008 Perspective—from genotype to phenotype: systems biology meets natural variation . Science 320, 495–497. (doi:10.1126/science.1153716). Crossref, PubMed, Google Scholar

Bluher M., Kahn B. B.& Kahn C. R.

. 2003 Extended longevity in mice lacking the insulin receptor in adipose tissue . Science 299, 572–574. (doi:10.1126/science.1078223). Crossref, PubMed, ISI, Google Scholar

Borash D. J., Rose M. R.& Mueller L. D.

. 2007 Mutation accumulation affects male virility in Drosophila selected for later reproduction . Physiol. Biochem. Zool. 80, 461–472. (doi:10.1086/520127). Crossref, PubMed, Google Scholar

Carbone M. A., Jordan K. W., Lyman R. F., Harbison S. T., Leips J., Morgan T. J., de Luca M., Awadalla P.& Mackay T. F. C.

. 2006 Phenotypic variation and natural selection at Catsup, a pleiotropic quantitative trait gene in Drosphila . Curr. Biol. 16, 912–919. (doi:10.1016/j.cub.2006.03.051). Crossref, PubMed, Google Scholar

. 1994 Evolution in age-structured populations. Cambridge, UK : Cambridge University Press . Crossref, Google Scholar

. 2000 Fisher, Medawar, Hamilton and the evolution of aging . Genetics 156, 927–931. PubMed, ISI, Google Scholar

. 2001 Patterns of age-specific means and genetic variances of mortality rates predicted by the mutation-accumulation theory of ageing . J. Theor. Biol. 210, 47–65. (doi:10.1006/jtbi.2001.2296). Crossref, PubMed, ISI, Google Scholar

Charlesworth B.& Hughes K. A.

. 1996 Age-specific inbreeding depression and components of genetic variance in relation to the evolution of senescence . Proc. Natl Acad. Sci. USA 93, 6140–6145. (doi:10.1073/pnas.93.12.6140). Crossref, PubMed, ISI, Google Scholar

Charmantier A., Perrins C., McCleery R. H.& Sheldon B. C.

. 2006 Quantitative genetics of age at reproduction in wild swans: support for antagonistic pleiotropy models of senescence . Proc. Natl Acad. Sci. USA 103, 6587–6592. (doi:10.1073/pnas.0511123103). Crossref, PubMed, ISI, Google Scholar

2008 Variations in DNA elucidate molecular networks that cause disease . Nature 452, 429–435. (doi:10.1038/nature06757). Crossref, PubMed, ISI, Google Scholar

. 1979 The biology of senescence. Edinburgh, UK : Churchill Livingstone . Google Scholar

Curtsinger J. W.& Khazaeli A. A.

. 2002 Lifespan, QTLs, age-specificity, and pleiotropy in Drosophila . Mech. Ageing Dev. 123, 81–93. (doi:10.1016/S0047-6374(01)00345-1). Crossref, PubMed, Google Scholar

de Luca M., Roshina N. V., Geiger-Thornsberry G. L., Lyman R. F., Pasyukova E. G.& Mackay T. F. C.

. 2003 Dopa decarboxylase (Ddc) affects variation in Drosophila longevity . Nat. Genet. 34, 429–433. (doi:10.1038/ng1218). Crossref, PubMed, ISI, Google Scholar

2008 Genetics of gene expression and its effect on disease . Nature 452, 423–428. (doi:10.1038/nature06758). Crossref, PubMed, Google Scholar

Escobar J. S., Jarne P., Charmantier A.& David P.

. 2008 Outbreeding alleviates senescence in hermaphroditic snails as expected from the mutation-accumulation theory . Curr. Biol. 18, 906–910. (doi:10.1016/j.cub.2008.04.070). Crossref, PubMed, Google Scholar

. 2006 The genomic rate of adaptive evolution . Trends Ecol. Evol. 21, 569–575. (doi:10.1016/j.tree.2006.06.015). Crossref, PubMed, ISI, Google Scholar

Eyre-Walker A., Woolfit M.& Phelps T.

. 2006 The distribution of fitness effects of new deleterious amino acid mutations in humans . Genetics 173, 891–900. (doi:10.1534/genetics.106.057570). Crossref, PubMed, ISI, Google Scholar

. 1990 Longevity, senescence, and the genome. Chicago, IL : University of Chicago Press . Google Scholar

. 2009 Environmental effects on sex differences in the genetic load for adult lifespan in a seed-feeding beetle . Heredity 103, 62–72. (doi:10.1038/hdy.2009.31). Crossref, PubMed, Google Scholar

Fox C. W., Scheibly K. L., Wallin W. G., Hitchcock L. J., Stillwell R. C.& Smith B. P.

. 2006 The genetic architecture of life span and mortality rates: gender and species differences in inbreeding load of two seed-feeding beetles . Genetics 174, 763–773. (doi:10.1534/genetics.106.060392). Crossref, PubMed, ISI, Google Scholar

Gavrilov L. A.& Gavrilova N. S.

. 1991 The biology of life span: a quantitative approach. Chur, Switzerland : Harwood Academic . Google Scholar

Gong Y., Thompson J. N.& Woodruff R. C.

. 2006 Effect of deleterious mutations on life span in Drosophila melanogaster . J.Gerontol. A Biol. Sci. Med. Sci. 61, 1246–1252. Crossref, PubMed, Google Scholar

. 1966 The moulding of senescence by natural selection . J. Theor. Biol. 12, 12–45. (doi:10.1016/0022-5193(66)90184-6). Crossref, PubMed, ISI, Google Scholar

Harbison S. T., Carbone M. A., Ayroles J. F., Stone E. A., Lyman R. F.& Mackay T. F. C.

. 2009 Co-regulated transcriptional networks contribute to natural genetic variation in Drosophila sleep . Nat. Genet. 41, 371–375. (doi:10.1038/ng.330). Crossref, PubMed, Google Scholar

. 1995 The evolutionary genetics of male life-history characters in Drosophila melanogaster . Evolution 49, 521–537. (doi:10.2307/2410276). Crossref, PubMed, ISI, Google Scholar

. 2005 Evolutionary and mechanistic theories of aging . Annu. Rev. Entomol. 50, 421–445. (doi:10.1146/annurev.ento.50.071803.130409). Crossref, PubMed, ISI, Google Scholar

Hughes K. A., Alipaz J. A., Drnevich J. M.& Reynolds R. M.

. 2002 A test of evolutionary theories of aging . Proc. Natl Acad. Sci. USA 99, 14 286–14 291. (doi:10.1073/pnas.222326199). Crossref, ISI, Google Scholar

Hunt J., Jennions M. D., Spyrou N.& Brooks R.

. 2006 Artificial selection on male longevity influences age-dependent reproductive effort in the black field cricket Teleogryllus commodus . Am. Nat. 168, E72–E86. (doi:10.1086/506918). Crossref, PubMed, ISI, Google Scholar

. 2001 Genetical genomics: the added value from segregation . Trends Genet. 17, 388–391. (doi:10.1016/S0168-9525(01)02310-1). Crossref, PubMed, Google Scholar

Keller L. F., Reid J. M.& Arcese P.

. 2008 Testing evolutionary models of senescence in a natural population: age and inbreeding effects on fitness components in song sparrows . Proc. R. Soc. B 275, 597–604. (doi:10.1098/rspb.2007.0961). Link, ISI, Google Scholar

. 1999 An experimental method for evaluating the contribution of deleterious mutations to quantitative trait variation . Genet. Res . 73, 263–273. (doi:10.1017/S0016672399003766). Crossref, PubMed, ISI, Google Scholar

. 2003 Deleterious mutations and the genetic variance of male fitness components in Mimulus guttatus . Genetics 164, 1071–1085. PubMed, ISI, Google Scholar

. 2008 Testing the rare-alleles model of quantitative variation by artificial selection . Genetica 132, 187–198. (doi:10.1007/s10709-007-9163-4). Crossref, PubMed, Google Scholar

. 2001 A conserved regulatory system for aging . Cell 105, 165–168. (doi:10.1016/S0092-8674(01)00306-3). Crossref, PubMed, ISI, Google Scholar

. 2005 The plasticity of aging: insights from long-lived mutants . Cell 120, 449–460. (doi:10.1016/j.cell.2005.02.002). Crossref, PubMed, ISI, Google Scholar

Kuningas M., Mooijaart S. P., van Heemst D., Zwaan B. J., Slagboom P. E.& Westendorp R. G. J.

. 2008 Genes encoding longevity: from model organisms to humans . Aging Cell 7, 270–280. (doi:10.1111/j.1474-9726.2008.00366.x). Crossref, PubMed, Google Scholar

. 2000 Quantitative trait loci for life span in Drosophila melanogaster: interactions with genetic background and larval density . Genetics 155, 1773–1788. PubMed, ISI, Google Scholar

Leips J., Gilligan P.& Mackay T. R. C.

. 2006 Quantitative trait loci with age-specific effects on fecundity in Drosophila melanogaster . Genetics 172, 1595–1605. (doi:10.1534/genetics.105.048520). Crossref, PubMed, ISI, Google Scholar

Lesser K. J., Paiusi I. C.& Leips J.

. 2006 Genetic variation in age-specific immune response in Drosophila melanogaster . Aging Cell 5, 293–295. (doi:10.1111/j.1474-9726.2006.00219.x). Crossref, PubMed, Google Scholar

. 1974 The genetic basis of evolutionary change . New York, NY : Columbia University Press . Google Scholar

Lin Y. J., Seroude L.& Benzer S.

. 1998 Extended life-span and stress resistance in the Drosophila mutant methuselah . Science 282, 943–946. (doi:10.1126/science.282.5390.943). Crossref, PubMed, ISI, Google Scholar

. 2007 Joint estimates of quantitative trait locus effect and frequency using synthetic recombinant populations of Drosophila melanogaster . Genetics 176, 1261–1281. (doi:10.1534/genetics.106.069641). Crossref, PubMed, Google Scholar

Mackay T. F. C., Roshina N. V., Leips J. W.& Pasyukova E. G.

. 2006 Complex genetic architecture of Drosophila longevity . Handbook of the biology of aging (eds

), pp. 181–216. Boston, MA : Elsevier . Google Scholar

Mackay T. F. C., Richards S.& Gibbs R.

. 2008 Proposal to sequence a Drosophila Genetic Reference Panel: a community resource for the study of genotypic and phenotypic variation . White Paper, NHGRI. See www.genome.gov/Pages/Research/Sequencing/SeqProposals/DrosophilaSeq.pdf. Google Scholar

Mackay T. F. C., Stone E. A.& Ayroles J. F.

. 2009 The genetics of quantitative traits: challenges and prospects . Nat. Rev. Genet. 10, 565–577. (doi:10.1038/nrg2612). Crossref, PubMed, ISI, Google Scholar

Martin G. M., Bergman A.& Barzilai N.

. 2007 Genetic determinants of human health span and life span: progress and new opportunities . PLoS Genet. 3, e125. (doi:10.1371/journal.pgen.0030125). Crossref, Google Scholar

. 1946 Old age and natural death . Modern Quart. 1, 30–56. Google Scholar

. 1952 An unsolved problem of biology . London, UK : H. K. Lewis . Google Scholar

Miller R. A., Berger S. B., Burke D. T., Galecki A., Garcia G. G., Harper J. M.& Akha A. A. S.

. 2005 T cells in aging mice: genetic, developmental, and biochemical analyses . Immunol. Rev. 205, 94–103. (doi:10.1111/j.0105-2896.2005.00254.x). Crossref, PubMed, Google Scholar

Moorad J. A.& Promislow D. E. L.

. 2009 What can genetic variation tell us about the evolution of senescence? Proc. R. Soc. B 276, 2271–2278. (doi:10.1098/rspb.2009.0183). Link, Google Scholar

Nuzhdin S. V., Pasyukova E. G., Dilda C. L., Zeng Z. B.& Mackay T. F. C.

. 1997 Sex-specific quantitative trait loci affecting longevity in Drosophila melanogaster . Proc. Natl Acad. Sci. USA 94, 9734–9739. (doi:10.1073/pnas.94.18.9734). Crossref, PubMed, ISI, Google Scholar

. 2008 Functional significance of allelic variation at methuselah, an aging gene in Drosophila . PLoS ONE 3, e1987. (doi:10.1371/journal.pone.0001987). Crossref, PubMed, Google Scholar

. 2002 Mechanisms of ageing: public or private? Nat. Rev. Genet. 3, 165–175. (doi:10.1038/nrg753). Crossref, PubMed, ISI, Google Scholar

. 2006 Beyond the evolutionary theory of ageing, from functional genomics to evo-gero . Trends Ecol. Evol. 21, 334–340. (doi:10.1016/j.tree.2006.02.008). Crossref, PubMed, Google Scholar

. 2007 Benchmarks for ageing studies . Nature 450, 165–167. (doi:10.1038/450165a). Crossref, PubMed, ISI, Google Scholar

Partridge L., Gems D.& Withers D. J.

. 2005 Sex and death: what is the connection? Cell 120, 461–472. (doi:10.1016/j.cell.2005.01.026). Crossref, PubMed, ISI, Google Scholar

Pasyukova E. G., Vieira C.& Mackay T. F. C.

. 2000 Deficiency mapping of quantitative trait loci affecting longevity in Drosophila melanogaster . Genetics 156, 1129–1146. PubMed, ISI, Google Scholar

Piper M. D. W., Selman C., McElwee J. J.& Partridge L.

. 2008 Separating cause from effect: how does insulin/IGF signalling control lifespan in worms, flies and mice? J. Int. Med. 263, 179–191. Crossref, PubMed, Google Scholar

Promislow D. E. L., Tatar M., Khazaeli A. A.& Curtsinger J. W.

. 1996 Age-specific patterns of genetic variance in Drosophila melanogaster. I. Mortality . Genetics 143, 839–848. PubMed, Google Scholar

Reynolds R. M., Temiyasathit S., Reedy M. M., Ruedi E. A., Drnevich J. M., Leips J.& Hughes K. A.

. 2007 Age specificity of inbreeding load in Drosophila melanogaster and implications for the evolution of late-life mortality plateaus . Genetics 177, 587–595. (doi:10.1534/genetics.106.070078). Crossref, PubMed, Google Scholar

. 1984 Genetic covariation in Drosophila life history: untangling the data . Am. Nat. 123, 564–569. (doi:10.1086/284222). Crossref, Google Scholar

. 1991 The evolutionary biology of aging. Oxford, UK : Oxford University Press . Google Scholar

. 1980 A test of evolutionary theories of senescence . Nature 287, 141–142. (doi:10.1038/287141a0). Crossref, PubMed, ISI, Google Scholar

Rose M. R., Rauser C. L., Benford G., Matos M.& Mueller L. D.

. 2007 Hamilton's forces of natural selection after forty years . Evolution 61, 1265–1276. (doi:10.1111/j.1558-5646.2007.00120.x). Crossref, PubMed, Google Scholar

Schmidt P. S., Duvernell D. D.& Eanes W. F.

. 2000 Adaptive evolution of a candidate gene for aging in Drosophila . Proc. Natl Acad. Sci. USA 97, 10 861–10 865. Crossref, Google Scholar

Shmookler Reis R. J., Kang P.& Ayyadevara S.

. 2006 Quantitative trait loci define genes and pathways underlying genetic variation in longevity . Exp. Gerontol. 41, 1046–1054. (doi:10.1016/j.exger.2006.06.047). Crossref, PubMed, Google Scholar

. 2005 Toward a unified theory of caloric restriction and longevity regulation . Mech. Ageing Dev. 126, 987–1002. (doi:10.1016/j.mad.2005.03.019). Crossref, PubMed, Google Scholar

. 2006 Inbreeding depression and male survivorship in Drosophila: implications for senescence theory . Genetics 172, 317–327. (doi:10.1534/genetics.105.045740). Crossref, PubMed, ISI, Google Scholar

Tatar M., Promislow D. E. L., Khazaeli A. A.& Curtsinger J. W.

. 1996 Age-specific patterns of genetic variance in Drosophila melanogaster. II. Fecundity and its genetic covariance with age-specific mortality . Genetics 143, 849–858. PubMed, Google Scholar

. 2006 Meeting report for the 4th annual complex trait consortium meeting: from QTLs to systems genetics . Mamm. Genome 17, 2–4. (doi:10.1007/s00335-005-0153-5). Crossref, PubMed, Google Scholar

Vieira C., Pasyukova E. G., Zeng Z. B., Brant H. J., Lyman R. F.& Mackay T. F. C.

. 2000 Genotype-environment interaction for quantitative trait loci affecting life span in Drosophila melanogaster . Genetics 154, 213–227. PubMed, ISI, Google Scholar

. 1957 Pleitropy, natural selection, and the evolution of senescence . Evolution 11, 398–411. (doi:10.2307/2406060). Crossref, ISI, Google Scholar

Wilson A. J., Charmantier A.& Hadfield J. D.

. 2008 Evolutionary genetics of ageing in the wild: empirical patterns and future perspectives . Funct. Ecol. 22, 431–442. (doi:10.1111/j.1365-2435.2008.01412.x). Crossref, ISI, Google Scholar


Watch the video: ΑΝΑΤΡΟΠΗ ΘΕΩΡΙΑΣ ΕΞΕΛΙΞΗΣ ΔΑΡΒΙΝΟΥ ΑΠΟ ΑΣΤΡΟΦΥΣΙΚΗ (May 2022).