Mutations would eventually lead to the extinction of a species

A Note: I have, indeed, not replied to the Kondrashov paper, which I do believe is the crux of Pro’s argument. This is in large part because so far ly been able to access the abstract, and thus do not know if Kondrashov answers his own question. C1: This point is of utmost importance. Firstly, if a mutation is beneficial or deleterious in regards to environment, and environment can change, that introduces a new variable into the question of whether or not a population will go extinct. Secondly, and as an addendum, there is a difference between recessive and dominant genes. For example, sickle-cell anemia is caused by two copies of a recessive allele. With this in mind, we might ask why it hasn’t been completely removed, or at the very least is far less common. The reason is simple—a single copy confers resistance to malaria[1]. The point to all this is that mutations are not nearly as clear-cut as Pro’s argument makes them out to be. The same mutation can be negative in one situation and positive in another, or it can be positive in conjunction with another mutation and negative without that mutation. There’s another point, too. In a population, (at the risk of simplifying) traits are selected against for two reasons: they do not replicate as well as their peers (examples, in species, can be seen in native species of frog in Australia, or some species of rat on an island in the middle of nowhere that I forget the name of), or they are so drastically unsuited for the area that they simply cannot survive (dinosaurs after the KT extinction). If everybody really is getting weaker, then one of the primary sources of selection isn’t going to affect the population. C2: Correction: 40% of mutations in a specific population of viruses were lethal (see Con’s source). These are also, for that matter, RNA viruses rather than DNA viruses, and humans have DNA rather than RNA. In lieu of another measurement regarding the percentage of harmful mutations in humans (since we are talking about humans, not RNA viruses), my study trumps. I might also add that while more recent studies are generally better, a true comparison should take into account things like sample size, sampling techniques, et cetera. C3: False. They could also be sterilized. Given the choice between total extinction (with severe suffering along the way) and sterilizing one third of the population, the latter choice seems like a valid alternative. In any event, not all captive populations are objectively bred. Namely, experimental populations are not (often) objectively bred. The same, to the best of my knowledge, applies to cricket/mealworm/fruit fly cultures bred for food (in the case of herptiles). This inevitably raises the question of why we don’t see such extinctions—even counting the delaying effect Pro mentions, given the vastly sped up breeding cycle, we would still expect to see Muller’s ratchet. C4: And yet about 20% of that DNA is still not known to serve any function, even with ENCODE’s data[2]. If mutations are randomly distributed, that means about 20% of the time a mutation has neither a beneficial or harmful effect. Another estimate puts it at 40% being useful, which means there is a 3/5 chance that a mutation has no significant effect[3]. C5: Speaking of Loewe, he also did another paper on Amazonian mollies. His analysis, using a simple model of Muller’s ratchet, found that Amazonian mollies, should, by all rights, have died out within the time period they are believed to have evolved[4]. Given that they very clearly haven’t, there are several explanations: The paleontological record is very, very, very wrong. Muller’s ratchet is incomplete, or at least the simple model is. There is something else avoiding Muller’s ratchet. Loewe hypothesizes the existence of the third. For instance, incorporation of DNA from sexual sister species and compensatory mutations could help to explain this. This is a common thread among papers discussing the concept. For instance, Michael Lynch, when discussing mutational meltdowns (a similar phenomenon)[5], noted that while mutational meltdowns (basically the same thing as Muller’s ratchet, really, at least for our purposes) that it is a serious risk for asexual populations—this is because ignoring back mutations, a parent experiencing no recombination of segregation can never produce offspring with fewer deleterious mutations than it carries. Recombination avoids this, by allowing two parents with deleterious mutations the possibility to produce offspring with fewer deleterious mutations. This is vitally important, because of the ‘best class’ of individuals in a population, there is always the chance that some will not reproduce or will produce progeny with new mutations, thus causing the class to be lost eventually. Erosion, if you will. P1: Recent data displays a germline bottleneck[6] in mitochondria, which has a net effect of resisting genetic decay. At the very least this can slow down Muller’s ratchet, but it could also potentially slow it down enough for beneficial mutations to keep mitochondria viable indefinitely. 1. http://en.wikipedia.org... 2. dx.doi.org/10.1126%2Fscience.337.6099.1159 3. http://www.genomicron.evolverzone.com... 4. http://www.biomedcentral.com... 5. http://www.indiana.edu... 6. http://pritch.bsd.uchicago.edu...