A New Run at the End of Evolution by Genetic Processes Argument

Hi, Faith.It’s been awhile* since the last time you and I debated (Reduction of Alleles by Natural Selection (Faith and ZenMonkey Only)), and I’m a bit disheartened to see that nothing has changed since then. *Five years already! Holy crap! I’ve had a second child, gotten my Ph.D., and completed a postdoc since then!I wanted to respond to a specific point you raised, and I’d actually like to respond to it using your own words from our last debate.Remember this: The example I had provided was from Hallet and Maxwell 1991 (see my post Message 47 for a quick overview of the salient details).And now, five and a half years later, you write this in your opening post: There was a brief moment, back in April 2010, where you really showed your colors: you admitted that evidence for beneficial alleles exists, but you decided to reject it anyway because all other mutations reported by evolutionists were just "assumptions" (despite the discussion I had provided upthread about the difference between "assumption" and "conclusion"). I remember how proud I felt that I was the one who had actually gotten you to admit that beneficial mutations exist, even if it ultimately proved to just be a momentary blip on your radar that you’ve apparently completely forgotten about. I’m sad, because I still look back on that debate with a lot of fondness, even though I still get a little twitch in my eye when I read the parts where my arrogance was showing.Ah well: it’s a long journey for all of us, isn’t it? I just wish I had been able to have a bigger impact on where your road was taking you than what I apparently have.Oh, and I never got that cookie you offered, either.Edited by Blue Jay, : Fix dateEdited by Blue Jay, : No reason given.Edited by Blue Jay, : No reason given.

Hi, FaithThis thread is already progressing pretty rapidly, so I was going to stay out of it to keep the clutter down, but I really want to comment on one point: This was part of the discussion that you and I had all those years ago: you’re using the word assumption wrong (see my Message 32 for the last time I explained this).When you observe a mutation that results in a different genotype and a concomitant new phenotype, as Hallett and Maxwell did way back in 1991, then you have evidence that mutations create new alleles.After that, if you then observe a new allele elsewhere, and attribute it to mutation, it is not an assumption. It’s a hypothesis, because it’s based on evidence. The evidence it’s based on is the verified observation of mutations causing new alleles.Does this mean that every allele necessarily originated from a mutation? No, of course not: there could be other mechanisms. We could propose that the newly-observed allele was created via spontaneous generation from free-floating nucleotides, and was not inherited from the parent organism at all. This proposal would be an assumption, because we do not currently have evidence that alleles can be spontaneously generated from free-floating nucleotides.We prefer to avoid unjustified assumptions, so we currently explain all alleles as the products of mutation. Admittedly, we could be wrong, but I find the evidence rather compellingly in favor of the theory that mutation alone explains all alleles. I guess time and more data will tell for sure, but until then, what else can I do beside accept what the evidence currently indicates to me?Do you understand why I believe that mutations are justified hypotheses, whereas spontaneous generation and Intelligent Design are unjustified assumptions?

Hi, Faith. Hypothesis, Faith. It is our hypothesis that ALL alleles in ALL genomes were formed by mutations. This hypothesis is based on the evidence that at least some mutations have been seen to form new alleles. It is not based on perfect evidence, because perfect evidence doesn't exist. But, there is evidence to support it. If a new mechanism for forming alleles is found, we can no longer accept that ALL alleles in ALL genomes were formed by mutations. But, since mutation is the only known mechanism for forming alleles, our working hypothesis is that mutation is the only mechanism.This is science, Faith. Science never really gets to an end result: it's always a work in progress, which means we're always basing our ideas on less evidence than we would like, and people like you think our incomplete and imperfect ideas are just "assumptions." It's terribly frustrating, and you might be able to imagine.

Hi, Faith. But it is science. -----Seriously, though: what's your alternative? On one hand, I could accept a hypothesis that's based on evidence that's not perfect, but still pretty good; on the other hand, I could... well, I'm not really sure what else I could do. Thoughts?Edited by Blue Jay, : No reason given.

Hi, Faith. Okay, so you didn't like my last post. I guess that wasn't the most productive decision I could have made. I just got excited about what I saw as a minor victory: you agreed to call it "science," instead of "assumption." I'll stop being juvenile about it if it helps us communicate.In all sincerity, I cannot understand how you and I can disagree on the things we disagree about. To me, using evidence about one thing to draw conclusions about other similar things seems perfectly reasonable, and this seems like the only thing I’m doing when it comes to alleles and mutations. But, to you, it apparently seems like a pile of wild assumptions and delusions.The contrast here is really jarring to me. You and I both think we’re being perfectly rational and making perfect sense, yet each of us thinks the other is being irrational. It reminds me of that one time when Bolder-dash and I both looked at the same photographs of apes and disagreed about whether the apes had facial hair. We couldn’t even agree on the facts contained in photographic evidence!I feel like I’ve made a good-faith effort to understand and explain, but I’m still having trouble identifying what keeps you from agreeing with my perspective on what is and what isn’t rational.Maybe it’s because I’ve only ever presented one paper on beneficial mutations? Maybe you think we only have one experiment that supports our idea that mutations create new alleles? Is that the problem?Just in case it is, here are a few more examples: Bacteria/MicrobesHere is a paper that used genetic markers to track adaptive events in a population of transgenic E. coli bacteria. They started with 1 single bacterial cell, and let it multiply over 1000 generations, periodically taking samples of the progeny and screening for mutations to a single target gene. They identified 66 mutations to that one focal gene which had an adaptive, or beneficial, effect on the fitness of individual bacteria. Here is a study that tracked changes in the ratio of two marker genes over hundreds of bacterial generations. Once they identified a population in which white- or red-marked bacteria had deviated from the starting ratio by a predefined amount, they calculated shifts in fitness by replicating the experiment and showing that either the white- or red-marked strain had indeed developed an adaptive advantage. They used these results to develop a mathematical model of the probability of a beneficial mutation reaching fixation. Here is a paper that identified 665 mutations in Pseudomonas fluorescens bacteria, and evaluated their fitness relative to the wild-type bacterium by comparative growth assays on a variety of different media. They discovered that the distribution of fitness effects was exponential, which means most of them had minor fitness effects, but a few of them had major fitness effects. Nematode wormsHere is a paper that discusses modern techniques for identifying phenotype-altering mutations in model organisms, including nematodes, plants and fruit flies. The specific mutation they focus on is a mutation that alters the developmental fate of stem cells in the nematode, Caenorhabditis elegans (this is a neutral phenotype). If you look through the references for this paper, you will find dozens of studies that talk about methods for screening populations of laboratory organisms for the presence of new phenotypes, and for identifying how each new phenotype is associated with a readily-identifiable mutation. ChickensHere is a paper that deals with mutations to pigmentation genes in chickens. The Dominant white allele does not occur in wild jungle fowl (i.e., wild chickens), but does occur in some populations of domestic chickens. Two mutations to the Dominant white locus include Dun and Smoky, both of which mutations have been positively identified. Furthermore, both of these mutants arose spontaneously in known populations, and the exact bird in which the mutation occurred is known. HumansHere is a short review paper about an allele in humans that has a beneficial effect on lipid transport. This allele is easily explained as a truncation mutation (i.e., a change to a single nucleotide creates a stop codon, which halts translation from RNA-to-protein early, resulting in a shortened protein). It’s occurrence within the human population suggests that it is not the ancestral condition, but a derived condition resulting from a single-nucleotide polymorphism. Here is a paper from 1984, in which large-scale screening of Jamaicans identified a family with a benign (i.e., neutral) phenotype variant that deals with the production of hemoglobin in humans fetuses. They were able to show that this phenotype was caused by a single point mutation, because they sequenced the genotypes of the child and the parents, and showed that the child’s genotype differed from both parents’. Here is a news article about a 2011 paper that used whole-genome sequencing on two families of humans, and determined that the children in both families have about 60 new mutations (relative to their parents), of which about 1 will have a phenotypic effect.-----I spent about 1 hour searching on Google Scholar with search terms like identifying beneficial mutations, and skimming/reading PDF’s, and I came up with 8 papers that show some really compelling evidence. These aren’t just lists of alleles that are purported to have been caused by mutations: these are mutations that have been observed directly, and have resulted in new alleles. Some of them are beneficial mutations, and none of the ones I reported are deleterious.How many more of these might I have found if I had spent an entire day on it? Even with a law of diminishing returns, I might easily expect to find a couple dozen experimentally-verified mutations, representing thousands of man-hours of experimental labor and millions of dollars of grant funding.When we say that alleles come from mutations, we aren’t making wild, unfounded assumptions. There really is very good evidence that alleles come from mutations, and a lot of scientists have put in a lot of hard work to acquire that evidence. And, there is no evidence that alleles come from anywhere else. Until that evidence comes out, mutation seems like the best --- indeed, the only --- hypothesis we’ve got.So, to me, it seems only rational to accept the mutation hypothesis until I see a good reason to think otherwise. Sure, it may turn out that I’m wrong: maybe some alleles come from some other mechanism, possibly even from an Intelligent Design mechanism, but if I accepted that now, with our current state of evidence, I would be making some unfounded assumptions, which we all agree are an inappropriate way to do scientific reasoning.Do you really, honestly, sincerely believe that this is irrational, or delusional, of me?Edited by Blue Jay, : No reason given.Edited by Blue Jay, : No reason given.

Hi, Faith. This cheetah story has been somewhat misrepresented, I think. The primary genetic bottleneck in cheetahs seems to date back to the Pleistocene (10,000 years ago), as this paper suggests, with modern anthropogenic effects having only exacerbated the problem. So recovery from this genetic bottleneck isn’t really the major consideration for conservation: rather, there is some concern that the cheetah may be unusually vulnerable to certain diseases. However, this paper found that at least one cheetah population shows evidence of having partially recovered its pre-bottleneck diversity at the immune-gene loci studied in that paper, and the unusually high rates of non-synonymous mutations indicates positive selection for increased diversity at these loci. To me, the couple of cheetah papers I just read seem to indicate that cheetahs have indeed accumulated new genetic diversity since their last genetic bottleneck. So, PaulK was at least partially correct: evolution has, indeed, continued after "total genetic depletion."The "as if nothing had happened to interrupt it" part is not supported by this data, but then I don't believe that accurately represents what PaulK said.-----One interesting thing to me is that, in the cheetah example, the effects of a severe genetic bottleneck seem to have carried over for 10,000 years or more. So, you're certainly right that reduction in genetic diversity can be a major obstacle to survival and later diversification of a population.But, my reading of the evidence suggests that mutation offers an avenue for adding new alleles, or a means of counteracting the depletion of diversity caused by selection. Even the cheetah example indicates that additive process of mutation can outpace the subtractive process of selection, and result in a net accumulation of alleles.Do you understand why I have come to this conclusion?

Hi, Faith. What if we "bloat our species with mutation-caused alleles" after the population has split into two separate populations?Couldn't we hypothetically accumulate enough new alleles via mutation that one of the daughter populations eventually ends up with higher allele diversity than the original, pre-split population had?

Okay, so you believe that mutations would allow for an increase in genetic diversity, but that it wouldn’t count as evolution. I would just say we could call it something other than "evolution" and leave it at that, but I don’t think your skepticism toward evolution only boils down to a semantic issue, so let’s try something else.Maybe let’s stop thinking of selection as an active process that reduces genetic diversity. Instead, think of it as a set of boundaries that constrain which mutations work and which ones don’t. So, the only mutations that accumulate are ones that fit within the constraints of the selection boundaries.The idea is that, when selection constraints are really stringent, fewer mutations can accumulate, so allele diversity will decrease.When selection constraints are really lax, more mutations can accumulate, and allele diversity will increase.That’s what we’ve been trying to explain about mutations outpacing or dominating natural selection and vice versa.Am I making sense yet, or do I still sound wrong to you?