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Seems to me that these two sources (M. Whitlock, B. Wallace) use different definitions of soft and hard selection.
M. Whitlock: Soft selection occurs when the relative fitness of an individual is calculated relative to the fittest individual of the local patch. Hard selection occurs when the relative fitness of an individual is calculated relative to the fitness of the fittest individual in the whole metapopulation.
B. Wallace: Soft selection occurs when the relative fitness of an individual is calculated relative to the fittest individual in the population. Hard selection occurs when the relative fitness of an individual is calculated relative a hypothetical fitness. Therefore, extinction only occurs under hard selection but never (except eventually when all individuals have fitness of 0) in the soft selection case.
Are there other definitions? What is the most common definition?
I think Wallace (1968) developed the ideas of hard and soft selection, as they relate to genetic load. He further explains the concept in Wallace (1975). As the idea was his, I'd go with Wallace's definition over Whitlock's. I haven't had time to watch the Whitlock video to see if they are saying more or less the same thing overall.
Consider a hypothetical population of individuals, each with 1000 loci (I'm basing example and ideas on an example given by Ridley 2004, pgs. 162-167). Heterozygotes at each locus has the greatest fitness (heterozygote advantage). Homozygotes at any locus will have reduced fitness. Therefore, the fitness of each genotype is given as:
Even if every individual in the population at time zero was heterozygous at each locus, Mendelian inheritance ensures that no individuals will be heterozygous at all loci after the second generation. Assume that fitness reduction at each homozygous locus is just 1%. Given that well over half of the loci will be homozygous, fitness of those individuals will be reduced to 0. They will die before reproducing. This is hard selection. If hard selection of this magnitude occurred in a population, then extinction would occur. This is what Wallace (in your link) is saying. This mortality due to the genetic load is added to the normal background mortality.
Soft selection compares the fitness of an individual to the genotype with the greatest fitness in the population, even if that genotype does not the theoretical optimum fitness. Soft selection replaces some of the background mortality with selective mortality, so the population size is not decreased overall.
Ridley, M. 2004. Evolution. 3rd ed. Blackwell Publishing, Malden, Massachusetts, USA.
Wallace, B. 1968. Polymorphism, population size, and genetic load. pp. 87-108 in R.C. Lewontin, ed. Population biology and evolution. Syracuse University Press, Syracuse, New York, USA.
Wallace, B. 1975. Hard and soft selection revisited. Evolution 29: 465-473.
What Is the Difference Between Hard and Soft Science?
The Science Council gives this definition of science:
The council goes on to describe the scientific method as being comprised of the following components:
- Objective observation
- Critical analysis
- Verification and testing
In some cases, systematic observation using the scientific method is a relatively straightforward process that can be easily replicated by others. In other instances, objective observation and replication can be difficult, if not impossible. In general, those sciences that can easily make use of the scientific method as described above are termed "hard sciences," while those for which such observations are difficult are termed "soft sciences."
Soft skills, on the other hand, are subjective skills that are much harder to quantify. Also known as "people skills" or "interpersonal skills," soft skills relate to the way you relate to and interact with other people. Soft skills include:
Unlike hard skills, it's hard to point to specific evidence that you possess a soft skill. If an employer is looking for someone who knows a programming language, you can share your grade in a class or point to a program you created using the language. But how can you show that you have a work ethic or any other soft skill?
Show, Don't Tell
Make note of your soft skills and point out some concrete instances where you've used them.
Just saying you have the skill isn't very meaningful. Instead, your best bet is to demonstrate that you possess this quality by sharing examples of times when you used it.
Watch Now: 6 Soft Skills Every Employer Wants
Citation: Rouzine IM, Coffin JM, Weinberger LS (2014) Fifteen Years Later: Hard and Soft Selection Sweeps Confirm a Large Population Number for HIV In Vivo. PLoS Genet 10(2): e1004179. https://doi.org/10.1371/journal.pgen.1004179
Editor: Christophe Fraser, Imperial College London, United Kingdom
Published: February 20, 2014
Copyright: © 2014 Rouzine et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This work was supported through an Alfred P. Sloan Research Fellowship (to LSW). The funder had no role in the preparation of the article.
Competing interests: The authors have declared that no competing interests exist.
Even among RNA viruses, which generally exhibit high evolutionary plasticity due to low fidelity of their RNA polymerases, HIV-1 is second only to HCV for its ability to generate within-host genetic diversity . HIV's rapid generation time leads to this high genetic diversity. The unfortunate consequences of HIV's rapid evolution are resistance to antiretroviral drugs , partial escape from immune responses –, the ability to switch tropism for target cells , and potential threats to new therapeutic strategies , . The forces driving and influencing HIV evolution include Darwinian selection, limited population size, linkage, recombination, epistasis, spatial aspects, and dynamic factors (particularly due to the immune response). These factors, and the parameters that define them, can be difficult to discern. One of the most elusive parameters critically important for the rate of evolution in every medically relevant scenario is the “effective population number” (Neff) (Figure 1). By definition, the census population size of HIV is the total number of infectious proviruses integrated into the cellular DNA of an individual at a given time. However, the genetically relevant Neff may differ substantially from the census population size. In this volume of PLOS Genetics, Pennings and colleagues  use new insights into “hard” and “soft” selective sweeps to estimate the effective population size of HIV.
For a number of reasons (see the text), the effective population may be much smaller than the census population.
The search for Neff (and other HIV evolutionary parameters) has gone on for almost two decades, following every turn and hitting each pothole on the eventful road of HIV modeling . The rapidity of resistance to monotherapy (in 1–2 weeks) was explained by the deterministic selection of alleles that preexist therapy in minute quantities . The large numbers of virus-producing cells (∼10 8 ) in the lymphoid tissue of experimentally infected macaques seemed to confirm this simple Darwinian selection model . However, the Darwinian view has faced challenges. Tajima's “neutrality test” applied to HIV sequences in untreated patients assumed that selection was neutral and predicted much smaller “effective” populations, of Neff∼10 3 . Since Tajima's approach was designed to detect isolated selective sweeps at one or a few mutant sites—while HIV exhibits hundreds of diverse sites in vivo—two groups re-tested the result. A linkage disequilibrium (LD) test  and analysis of the variation in the time to drug resistance  arrived at the same value, Neff = (5–10)×10 5 , for an average patient (with the mutation rate ∼10 −5 per base). Such populations are sufficiently large for deterministic selection to dominate, yet not large enough to neglect stochastic effects altogether. The LD test  is affected by recombination, and HIV's recombination rate had not been well measured at that time. The recent measurement of 5×10 −6 crossovers per base per HIV replication cycle in an average untreated individual – updates Neff to (1–2)×10 5 , not far from the original value. A recent study of the pattern of diversity accumulation in early and late HIV infection confirms the range of Neff . However, all these estimates of Neff are lower bounds.
Pennings et al.  continue this quest for an effective population size of HIV using a new method based on a theoretical calculation of the probability of multiple introductions of a beneficial allele at a site before it is fixed in a population . The prediction does not depend on whether mutations are new or result from standing variation prior to therapy. The authors use sequence data obtained from 30 patients who failed suboptimal antiretroviral regimens, including efavirenz —a non-nucleoside reverse transcriptase (RT) inhibitor (NNRTI)—and who exhibited a rise of drug-resistant alleles in RT. The sequence data reveal fixation of two alleles, both corresponding to an amino-acid replacement K103N. Pennings et al.'s analysis focuses on the genetic composition at RT codon 103 and the adjacent 500 nucleotides. Based on the changes in the genetic diversity in this region, 30 fixations are classified into “hard” selective sweeps with a single parental sequence, or “soft” sweeps with multiple parental sequences. Observing that both types of sweep occurred at similar frequencies (also confirmed by observations in other resistance codons), the authors predict Neff = 1.5×10 5 , in agreement with the LD test.
Pennings et al. also discuss why “selectively neutral” methods based on synonymous diversity underestimate the population size. It is well known that a selection sweep lowers the diversity at linked sites (hence the term “sweep”) and any method assuming selective neutrality translates lower diversity to smaller Neff. The interesting part is the dynamic component of this effect. Pennings et al. demonstrate that rapid sweeps are followed by long periods when the diversity recovers at the linked sites (for synonymous sites, these periods are very long). From another angle, we can add that selection shortens the time to the common ancestor, which decreases the sequence divergence. The ancestral-tree argument is rather general and also applies to a large number of linked sites evolving under selection –.
The previous estimates , ,  were lower bounds on Neff. In contrast, the Pennings et al. study puts a number on Neff. However, this number (Neff = 1.5×10 5 ) raises a question: why is Neff so far below the census population size of 10 8 or more? Pennings et al. offer an elegant explanation of this relatively small Neff in the spirit of the “traveling wave” approach –. They note that resistant alleles at different sites emerge against different fitness backgrounds. To be fixed, alleles conferring a small benefit must emerge in the most-fit genomes ,  hence, the effective Neff for these alleles is small. Alleles with a larger beneficial effect can explore a larger fraction of population (larger Neff). Conceptually, this idea is quite correct quantitatively, in the context of drug resistance, some problems arise. For example, the fitness benefit from a resistance mutation (under drug) is almost 100%, while the difference between the fittest and the average genome (in untreated patients) is a modest ∼10% . Indeed, the average selection coefficient is quite small, ∼0.5% , .
There may be several other reasons for Neff<10 8 , as follows.
- By considering only 500 bases (∼5%) of the HIV genome, the study may underestimate the number of genetic backgrounds in which the resistant allele can be observed.
- Neff is likely to vary in time—similar to viremia, which decays strongly after the onset of therapy and rebounds after its failure—and the placement of the inferred population size within the therapy time frame is unclear. Specifically, it is unclear from the empirical source  whether K103N mutations are generated before therapy (which is likely, considering that the mutation of interest decays very slowly in vivo in untreated patients and therefore has a low mutation cost ) or after therapy fails for another reason (see Figure 1 in ). In the first scenario, inferred Neff = 10 5 is the pretreatment number. In the second scenario, the pretreatment number must be much higher than 10 5 , since the replicating census population is reduced by a large factor (∼100) following initiation of therapy.
- Other factors, such as variation of the population number among patients and the spatial organization of the infected tissue  (both neglected in the test), may be relevant. Furthermore, the authors' calculations rely on the assumption of equal mutation rates for the two resistance mutations analyzed (both transversions). If the underlying rate of AAA to AAC is much greater than that of to AAT, the cited analysis would have underestimated the frequency of soft sweeps, yielding an underestimate of Neff.
- A significant complicating factor is the presence, in the parent study , of other drugs, particularly the nucleoside RT inhibitors (NRTIs) AZT and 3TC. In some cases, mutations conferring resistance to these drugs may have also contributed to failure (e.g., during the precursor monotherapy see Figure 1 in ), and the requirement for these additional changes would have made the frequency of resistant strains much less than the estimate. For virus that escaped the combination treatment in the absence of NRTI mutations, replication was most likely occurring only in a fraction, or “sanctuary,” of cells that did not receive an inhibitory dose of these drugs. Either or both of these effects would have led to a potentially large underestimate of Neff. Indeed, a recent study of rapid NNRTI resistance, in SIV-infected monkeys treated with efavirenz monotherapy, used an ultrasensitive PCR assay to estimate the pre-therapy level of either K103N mutation as less than 0.0001% , implying a total replicating population of >10 6 .
For these reasons, the value Neff = 1.5×10 5 obtained in the study of Pennings et al. should probably still be regarded as a lower bound. At the same time, the study solidifies our understanding of HIV evolution as a Darwinian process and leads to important questions regarding the structure of HIV population, which are still waiting for new insights.
Kin Selection and Parasite Evolution: Higher and Lower Virulence with Hard and Soft Selection
Conventional models predict that low genetic relatedness among parasites that coinfect the same host leads to the evolution of high parasite virulence. Such models assume adaptive responses to hard selection only. We show that if soft selection is allowed to operate, low relatedness leads instead to the evolution of low virulence. With both hard and soft selection, low relatedness increases the conflict among coinfecting parasites. Although parasites can only respond to hard selection by evolving higher virulence and overexploiting their host, they can respond to soft selection by evolving other adaptations, such as interference, that prevent overexploitation. Because interference can entail a cost, the host may actually be underexploited, and virulence will decrease as a result of soft selection. Our analysis also shows that responses to soft selection can have a much stronger effect than responses to hard selection. After hard selection has raised virulence to a level that is an evolutionarily stable strategy, the population, as expected, cannot be invaded by more virulent phenotypes that respond only to hard selection. The population remains susceptible to invasion by a less virulent phenotype that responds to soft selection, however. Thus, hard and soft selection are not just alternatives. Rather, soft selection is expected to prevail and often thwart the evolution of virulence in parasites. We review evidence from several parasite systems and find support for soft selection. Most of the examples involve interference mechanisms that indirectly prevent the evolution of higher virulence. We recognize that hard selection for virulence is more difficult to document, but we take our results to suggest that a kin selection model with soft selection may have general applicability.
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Function of Skeleton
For vertebrates such as humans, the skeleton performs many essential functions. Some are directly related to the purpose of all skeletons of providing structural support, protection, and support for locomotion. Others are biological functions unrelated to structural support that have been adopted by vertebrate bone tissues over time.
The functions of the skeleton include:
The skeleton serves the vital purpose of giving form to an animal’s body. Some animals that live in water, such as the octopus, have no skeleton. This is possible because their tissues are partially supported by the water that surrounds them, which is much heavier than air and allows some of an animal’s body structures to float. You’ll notice that octopi don’t do so well on dry land!
For land animals, it’s essential to have a skeleton that fights the force of gravity, which might otherwise prevent movement and even crush organs. That’s why all mobile land animals have either an exoskeleton, like those of insects and spiders, or an internal skeleton, like those of humans and other vertebrates.
Almost all forms of on-land locomotion require the ability to push rigid levers against our environment. When we walk, our leg bones are levers that exert force on the ground to propel us forward. When birds fly, their wing bones are levers that push against air molecules to allow them to move.
The role of bones in locomotion is the major reason why broken bones can be a death sentence for animals in the wild. Without intact levers to push against, animals can be unable to move quickly or at all, which in turn renders them unable to find food or escape from predators.
In addition to supporting the body’s structure against the force of gravity and allowing locomotion, the skeleton plays the vital role of protecting important organs from injury. Some important protective bones in the human body include:
- The skull is a thick covering of bone that protects the brain from injury.
- The spinal column – made of “vertebrae,” from which “vertebrates” get their name – protects the spinal cord, which is the major nerve cord that allows the brain to communicate with the body.
- The ribcage forms a protective barrier around the lungs and heart, without which the body would not be able to supply blood to the brain and would soon die.
The vertebrate body must make compromises between protection and mobility. Our lower abdominal organs such as the intestines, for example, are not protected by the ribcage. But this lack of a hard covering around our abdomen allows us to bend climb, and shift our weight in a way that greatly enhances our mobility!
Blood cell production
For animals with internal skeletons, the bones also perform other vital biological functions that are not directly related to their role as structural support. In humans, one of the most important of these roles is blood cell production.
Our bones are made out of living tissue. Their outer tissues are hard and rigid, but their inner tissues are soft and serve other purposes. On the inside of our bones – in the part called the “bone marrow” – the stem cells that create our red and white blood cells can be found.
Without healthy bone marrow, our bodies would stop replacing their blood cells – and would soon lose the ability to transport oxygen and fight infection!
This is why bone marrow transplants are sometimes prescribed for people with “blood cancers.” In blood cancers such as leukemia, the cancerous cells actually originate in the bone marrow. These cancerous cells produce large numbers of blood cells, but the blood cells they produce do not work properly.
As a result, people with cancer of the stem cells that produce white blood cells may have very high white blood cell counts – but they have difficulty fighting infection, because these white blood cells produced by cancerous stem cells do not work properly.
In bone marrow transplants, doctors attempt to kill off the stem cells in a patient’s own bone marrow, and then replace some of the marrow with marrow from a healthy donor that can produce healthy blood cells.
Bones can store calorie-rich fat and minerals that other body tissues might need at a later date.
The hard part of bone tissue is rich in calcium, which in emergencies the body can release from the bones to serve other purposes.
Yellow bone marrow tissue is composed primarily of fat, which can act as a storage point for calories and nutrients.
Red bone marrow tissue is rich in iron, a necessary ingredient for red blood cells. Iron deficiency is a common cause of anemia – a condition in which insufficient production of red blood cells can lead to weakness, fatigue, dizziness, and even fainting.
Bone cells release a hormone called osteocalcin, which has effects on blood sugar, fat storage, and male sex hormones.
The release of osteocalcin by bone cells prompts the pancreas to release more insulin, resulting in lowered blood sugar and increased consumption of sugar by cells. It also causes fat cells to release a hormone called adiponectin, which prompts the breakdown of fat for energy.
Osteocalcin directs the male testes to produce more testosterone, and is also thought to encourage the body to produce more bone cells.
The complex interplay between hormones in the human body is not well-understood. In this case, it’s possible that by prompting the release of insulin and the breakdown of fats for energy, it may be freeing up additional energy that the body can use to grow more bone cells.
OR THIS: (KNOTTED BONES)
What makes our bones hard? That's right! Calcium carbonate -- the same thing that made the egg shells hard.
Take some thin chicken bones and drop them in vinegar for a day. Take them out and they'll be soft just like the egg shells were.
Now you can tie them in a knot, just like a piece of string.
Leave them sitting out on the table and they'll get hard again!
Take them to school for sharing time and see if your classmates can figure out how you did it (or do this at school and take them home to stump mom and dad!)
Putting It All Together
The most important thing to remember is to select skills that are relevant to the position you are interviewing for, and more important than that, skills that your company puts a tremendous amount of value in.
Once you get your skills straightened out, you should make sure that the rest of your resume is congruent with the skills you just selected, namely, that your experience shows that you both used those skills in a work environment and developed the skill with on-the-job tasks.
The next thing you should do is download our action list below!
Interviews with Animal Groups
Jamarion Gallaway on November 08, 2019:
guess who i like yall khalia and shakalya williams and Adrin and tymia and darryl because they so black and i like dark chocolate people periot pooh.
Shakayla williams on November 07, 2019:
awww yall so cute tyte and adrin
what. on November 07, 2019:
janaya on November 07, 2019:
Darryl on November 07, 2019:
tymia on November 07, 2019:
Adrin Avery on November 07, 2019:
adrin A on November 07, 2019:
Jay on November 07, 2019:
deaundre on November 07, 2019:
kendra johnosn on November 07, 2019:
Tyteonaa on November 06, 2019:
tymia on November 06, 2019:
Rianne on October 07, 2019:
I like fish is this a free website
man on June 07, 2019:
i once saw a reptile kickflip on a scooter before, razer to be specific.
El mas crack on March 19, 2019:
timmy on November 01, 2018:
Timmy on November 01, 2018:
chris on November 01, 2018:
kyler on November 01, 2018:
i will be the last one to comment
braden on March 15, 2018:
I think reptiles should WIN!REPTILES RULE!
Yameen on March 12, 2018:
Thanks that is very useful to use.thank u
Vikas on January 05, 2018:
This is very helpful for me and thnx
samyah on September 28, 2017:
jalylah on September 28, 2017:
so mammals really and only 9 on reptiles
kaleigh on August 21, 2017:
Charles on October 21, 2016:
shasha on March 24, 2015:
its very good for kids and my son loves it
ashin on March 24, 2015:
Oliver on March 03, 2015:
I fond it exa leant and fun keep it up
mervin apostol on August 07, 2014:
my crush is_________________________________
Aminallover on April 17, 2014:
Hello how do I reference this? What is the name of the author and year?
vibesites from United States on October 18, 2012:
Very interesting and absolutely educational, and recommended for students and little kids who are interested in biology. :)
Marcy Goodfleisch from Planet Earth on September 26, 2012:
Very nice hub, and so instructional for kids! I love the photos you included here!
Rhys Baker (author) from Peterborough, UK on September 19, 2012:
Yeah..I tried finding out some more and struggled. How I wish I had my uni papers access again.
I have a first class degree in Biology with a specialism in Toxicology and Cell Biology and a Teaching Certificate in Secondary Science.
I was arguing with my dept. head about the tongue map - she was adamant there were discrete regions until I showed her the changes. It actually makes sense. If you put something sour on the tip of your tongue, it tastes sour if you put something sweet on the tip of your tongue it tastes sweet. I have no clue what unami is. :)
Lena Welch from USA on September 18, 2012:
I would agree with you on that one. I think the only reason I learned it was that my professor did a dissertation on birds. Finding the pages for you was hard. I had to look up monophyletic groups and birds and birds and cladistics.
A lot of education in the classroom is slow. A few weeks ago I learned that the taste bud maps were incorrect and they have known since 1974 - and it is still in classrooms!
What is your degree background?
Rhys Baker (author) from Peterborough, UK on September 18, 2012:
More to the point it shows how far education lags behind these discoveries - it seems the reclassification of reptilian occurred in 2004. This wasn&apost mentioned in my degree lectures, even as late as 2010!
It doesn&apost seem that this classification change is going to filter down below uni study as the change is so technical that birds and reptiles remain as two essentially separate groups only linked by a common ancestor that therefore requires both descendants to be recognised in the same Clade. It also seems to defy common sense for the traits that I previously listed. But you are right - it is fascinating. if highly technical!
Lena Welch from USA on September 18, 2012:
Aww the computer booted my edited comment with the easier to read article: http://www.ucmp.berkeley.edu/diapsids/avians.html
Lena Welch from USA on September 18, 2012:
Here is a great page explaining the phylogeny of animals. It shows the cladograms with birds as a type of reptile and explains why current thinking is placing birds with crocodiles.
It is interesting to look at and really shows how much our views in science are still changing, even in areas that were once thought to be fairly absolute. Thus we get avian and non-avian reptiles.
Rhys Baker (author) from Peterborough, UK on September 18, 2012:
It would surprise me if birds were considered reptiles due to huge differences between them (birds are homeothermic, lay hard shelled eggs, have no teeth, possess a beak and are covered in feathers not scales) iamaware that research is revealing that they are much closer related to dinosaurs than we ever thought. But this doesn&apost make them reptiles. Scales, leathery eggs and polikilothermy would make them reptiles.
Nettlemere from Burnley, Lancashire, UK on September 18, 2012:
I can&apost vote for my favourite I like them all. Great hub though, ideal for biology classes and general interest.
Lena Welch from USA on September 17, 2012:
Interesting article as I just did this in Bio 175. Did you know that birds are now considered reptiles?