Reduction of Alleles by Natural Selection (Faith and ZenMonkey Only)

GREAT DEBATE: FAITH AND BLUEJAY ONLY!I would like to continue the discussion Faith began in The End of Evolution By Means of Natural Selection in the Great Debate forum, if she is interested in continuing it.I’ll focus my comments on this portion of her OP there: This topic has caused a lot of frustration (primarily for Faith herself), so I’ll try to tread softly and take it easy. I’ll provide a basic comment on each sentence from the above quotation: these will serve as prompts that can be used by Faith to start her side of the discussion however she chooses.Faith, please let me know what I may have misunderstood from your statements, and help me find if and where I'm off base on any or your points. I can only address this statement by appealing to mutation, which is known to happen at extremely higher rates than natural selection happens. If mutation is disallowed, then this statement may very well be quite true.However, if mutation is allowed, then it becomes a question of comparing the rate of selection-mediated diversity loss to the rate of mutation-mediated diversity gain.Do you agree with that?----- For this one, we need to consider a timeline of events, including the following events:

1. Onset of selection pressure
2. Emergence of new alleles
3. Extermination of alleles selected against

And, the following considerations:

1. Other concurrent selection pressures
2. Genetic linkage between different alleles
3. Magnitude of each selection pressure

If we choose to pursue this complex model, I think we’ll quickly find that decreasing genetic diversity is not so inevitable as you have argued. I'll hold off on the specifics until you're ready to discuss it.----- I explained a bit about genetic fixation in a few other places. Fixation is what you’re talking about: the elimination of all alleles for a certain gene except for one.I do not think that fixation is inevitable, and I’m certain will never occur at all positions in the genomes of all individuals within a single population.Selection pressures simply cannot be orchestrated such that any single organism can contain all the best alleles for all genes: so, naturally, we should expect that no single combination of alleles will be absolutely superior to all other possibilities in a population.As an example, let me present Uta stansburiana, the rock-paper-scissors lizard I referred to earlier in your thread. This is an (admittedly unusual) example of a population that has reached a relatively stable balance between different genotypes. This sort of balancing act is what is going on in nearly all populations, all the time: the equilibrium oscillates between different character states, occasionally leading to the complete extinction of a certain trait, but also often leading to a complete rebound of a rare allele.-----I look forward to your responses, and I hope I won’t upset you and frustrate you too much in our discussion.Edited by Bluejay, : Some reformatting, "do you agree with that?" and "I'll hold off on the specifics until..."Edited by Bluejay, : Alter title in accordance with Faith's wishes.Edited by Bluejay, : No reason given.Edited by Admin, : Change title now that ZenMonkey is taking over for Bluejay.

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.

Hi, Faith.I've altered the title in accordance with your preferences. I agree: let’s take our time on this, and make sure we’re communicating effectively.In that spirit, I wanted to ask for a bit of elaboration/clarification: How do you envision new traits emerging? Not by mutation, I gather?Having traits and alleles show different diversity patterns seems contradictory to me. Granted, there isn’t a one-to-one correlation between allelic diversity (you can have some traits that emerge without new alleles emerging, and you can have new alleles emerge without producing any new traits), but I would think that there should be a general trend of correlation between allelic and trait diversity, given that all traits ultimately trace back to alleles.I’m also uncertain as to how trait diversity is increasing in your scenario.I would appreciate any explanation or clarification on this point. Take whatever time you need or want to do so.-----In the meantime, perhaps a bit of terminology would be beneficial, just to make sure we’re both clear on what we’re talking about:gene: a region of the genome that encodes a certain product
allele: one of several sequence variants of a genecharacter: a physical attribute of an organism
trait: one of several variants of a charactergenotype: a suite of alleles in a single organism
phenotype: a suite of traits in a single organismAlso, are you familiar with the mechanisms of mutation and evolutionary genetics (e.g., crossing over, independent assortment, point mutations, insertions/deletions, etc.)? We might not need to talk about these, but, just in case...-----I look forward to this: it’s going to be fun. Except, now it seems that we're going to have an audience with commentary privileges. I hope I don't get camera-shy.

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.

Hi, Faith. I think you’re expressing yourself just fine: it’s perfectly coherent and it’s a great basic explanation of the process of natural selection.My only point of confusion is why you think this process will inevitably lead to complete allele depletion. I think that’s going to be too big a question to try to tackle in one step, so let me ask a simpler question (and a follow up):Do you agree that, if mutation is allowed, then new mutations can, at least in principle, produce new alleles?If so, doesn’t basic reasoning tell us that the change in diversity can be determined by comparing the number of new alleles produced by mutations to the number of old alleles exterminated by natural selection?-----Keep in mind, we’re still just considering one gene here. I don’t want to get into a multiple-gene scenario until we’ve cleared up how to measure changes in diversity for one gene.

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.

Hi, Faith.Let me clear up a couple managerial type things here. I’ll post a response to the meaty portions of your post in a second reply to follow shortly after this one. I humored you on the title.selection doesn’t work on alleles, it works on traits. If an organism has camouflaged coloration, natural selection doesn’t care if its genotype is Aa or AA. So, the only thing natural selection can actually reduce directly is traits. Because alleles are the cause of these traits, natural selection working on these traits will necessarily impact the alleles, too.There really wasn’t anything wrong with the title I proposed: it said exactly what I wanted it to say. I changed it because I wanted to avoid this little discussion until the Great Debate had been agreed upon and established. On a somewhat related note, I also apologize for not having posted a message at your topic informing you of this debate (that’s standard etiquette). I wanted to wait until was promoted, but, by then, Percy had already posted the note.----- A thread with two wordsmiths can be extremely trying on everybody’s patience. This is me talking from personal experience. I had originally written extinction, and then thought better of it and switched it to depletion, which is a slightly softer word that still conveys a similar idea. Unfortunately, I forgot to edit out complete. I guess reduction could be seen as slightly softer than depletion, but I don’t see a meaningful distinction to be made there, and my usage of depletion wasn’t intended as anything different from your usage of reduction.Let’s just agree not to get too picky about semantics outside of the usage of well-established terminology (trait, allele, gene, etc.): I think we’ll both be happier that way.----- Well, no you didn’t: I was only referring to my own post. I’ll remember never to use the royal we outside of my kingdom again.

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.

Hi, Faith. You may be going too fast for me now! My next response may be somewhat less soon than I anticipated. I should be able to get it out tonight sometime.Thanks.

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.

Hi, Faith.I was going to make a detailed, step-by-step response to all of your points, but I think it would be more effective to focus on just the elephant in the room, now that I am aware that it's there. This contradicts the main point of your argument, and is really the crux of the argument I’ve been trying to bring against you.You have been arguing that natural selection should eliminate most of the genetic diversity in a population. You have a parent population with all kinds of allelic diversity in a model where allelic diversity is inexorably reducing over time. So, why shouldn’t this process also be working in the parent population? What is different about the parent population that allows it to maintain high levels of genetic diversity?Edited by Bluejay, : No reason given.

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.

Hi, Faith.I'm currently a doctoral student in an entomology program. Specifically, I'm work in spider ecology.

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.

Hi, Faith. That's what I thought. However, this makes the situation into a game of numbers, a math problem, to which you have strenuously objected all along.You seem to accept that numbers and rates of change will have something to do with the problem, but you won’t accept any pro-evolution arguments that have anything to do with rates. Then, when you make comments like this--- ---it comes off as if you’re just arbitrarily choosing what variables can and can’t be included.I have twice referenced a paper that found approximately 60 new mutations in the genomes of two human children. If we assume 1-2% of the genome is coding DNA (i.e. genes), this means we should expect 1-2% x 60 = 0.6 new alleles per individual birth (this is genome-wide).Why is this not evidence for mutations?
Why should mutations be simply left out of the model?----- And, in the scenario you're addressing, this makes perfect sense. But, the evidence I have presented suggests that reality does not conform to the scenario you want to address. So, naturally, I have been trying to convince you that you should address a different scenario from the one you want to address.

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.

Hi, Faith. So, why did you make such a big deal about the title, then?

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.

Hi, Faith. I've got no objection to your debate style or posting style at all. I won't be able to (or interested in) responding to everything you post, but I have read essentially all of it. Go ahead and keep posting however frequently and however much you want to: I'm sure you and I aren't the only ones reading this.My next response is nearly complete: it's taken me all day because I've had to work around several church meetings, Easter celebration with visiting family members, entertaining the baby and putting him to bed, and cleaning up afterwards.I think I'm almost ready. Thanks for your patience.

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.

Hi, Faith.Here, I'm going to deviate a bit from my pattern so far. I'm not going to respond directly to any of the points you've been saying: I'm going to present a detailed counterpoint, starting with this prompt: I understood exactly what you said the first time you said it. In fact, your argument is really an old concept, dating to the 1950’s in genetics, and is a concept I learned about in my undergraduate genetics courses. There is a name for it: the Founder Effect.It generally combines three basic, interrelated evolutionary concepts: (1) genetic bottlenecks; (2) allopatric speciation (i.e., speciation by physical isolation); and (3) genetic drift.It is a well-documented and well-known phenomenon. You identified several key examples of it (seals, cheetahs, etc.), and nobody is disputing that it happens, that it can have major consequences on a population, or that it reduces genetic diversity in that population.Once again, all that is being disputed is the universality of your argument. I personally dispute the universality of your argument on two fronts: (1) the time it takes to kill a species after it passes through a bottleneck; and (2) the well-documented evidence for the occurrence of diversity input into the system (i.e. mutations).-----As an example, let’s consider the Northern elephant seal. According to the Wiki article, they reached their low point (total population less than 1000 individuals) in the late 1800’s/early 1900’s. With the help of hunting bans, in the roughly 100 years since, their population has increased to over 100,000.They reached a severe genetic bottleneck over a century ago, but are not extinct yet. Let’s try to apply the human mutation rate to the elephant seals and see what their genetic diversity is like today (don’t worry: I’m not particularly mathematically inclined, either---as you can see by my math needing to be clarified by Admin).So, let’s use 0.6-per-individual as the rate of new alleles in the population (it's friendlier to your argument than Percy's figure). Thus, we should estimate that there are approximately (100,000 individuals x 0.6 new alleles/individual) = 60,000 new alleles among the currently living elephant seals, without considering all the individuals that lived and died and mutated in the interim. If elephant seals have roughly the same number of genes as humans (22,000), that means they should average almost 3 new alleles per gene (granted, some genes will have mutated much more or much less than this, so this average may be pretty much a meaningless number).Many of these new alleles will not be passed on to the next generation, and many others are at such low levels as to be effectively irrelevant to the current gene pool. But, with so many tens of thousands of new alleles having been introduced, what are the chances that none of them is catching on? What are the chances that none of them will alter (or have altered) the patterns of natural selection in the population?Perhaps more to the point, how long is it going to take for this depleted gene pool to finally implode under the pressures of natural selection? All indications are that these seals are fully capable of persisting long enough to see their population’s genetic diversity return to a healthy level by means of subtle, gradual accumulation of random mutations.So, why should we think that reduced genetic diversity is, in principle, an insurmountable obstacle in all evolutionary scenarios? It looks to me like this is far from a foregone conclusion.

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.

Hi, Faith.I think the mood of the thread suddenly turned icy, and I'm pretty sure I didn't do anything to deserve it.Why don’t we slow down? I’m going to restrict myself to one post a day: maybe that will help keep the passion and frustration out of it. What's to stop a beneficial mutation from happening?
The effects of a mutation on the organism have nothing to do with the mechanism that causes the mutation; so benefit or detriment cannot possibly have impacted the occurrence of the mutation.By analogy: People can walk. But, it's an assumption imposed by evolutionary theory that people can walk to a watering hole to get water. This makes no sense!Unless there is some mechanism that would prevent any particular nucleotide from changing to a "better" nucleotide, there is no reason to think beneficial mutations can't occur.The only reason to propose such a thing is if you are assuming that the way things currently are is already optimal, and cannot be improved upon. My personal work in ecology tells me that to assume such would be very inappropriate: the behavior of most organisms is not particularly optimal or efficient.----- Science learns and grows all the time.If the people 100 years ago had had the foresight to take genetic samples back when the seals were almost extinct, maybe we could learn something about genetic bottlenecks and subsequent recoveries today. But, at that time, they weren’t even aware of what function DNA performed. All we can really do is learn to do it right in the next study.If you’d like, when I become a full professor (that will take more than 10 years, probably), I can write a grant, and you and I can go sequence elephant seal genomes together. Of course, my grant will probably get rejected, because not only is research funding for non-applied stuff getting whittled down to nothing, but I do not have, and probably never will have, the credentials to work with elephant seals or genome-sequencing technology. Sorry to disappoint you, but the best I can do is wait for seal people to do the work themselves.But, in the meantime, I’ve already presented a paper that used modern genetic techniques to compare the whole-genome sequences of children to their parents, and it showed that 60 was a rough average for the number of mutations per individual. To my knowledge, this is the first time such an experiment has been done. It's hard, expensive work to sequence an entire genome to look for mutations, let alone to sequence the genomes of multiple individuals for comparison. Now that it’s got precedent, and the tools are becoming more accessible, I’m sure we may be seeing more of it soon, and many examples of new alleles will start coming forward.However, the only practical way to study mutations currently is to look for gross disfigurement in fruit flies or Arabidopsis plants and try to see if there is a genetic basis for the disfigurement. This is hardly conducive to assessing the rates of beneficial mutations, so it shouldn’t surprise anybody that we rely on correlative field data.But, for now, all the data we have collected suggests that there is no reason to deny the possibility of beneficial mutations, and no reason to think that genetic bottlenecks are insurmountable to biological populations. There is only data that is favorable to the possibility that the genetic diversity of a population can increase over time.----- You think I did it for libel?I did it because I saw it as the only way to get you to stop thinking you have to repost the basic description of your argument in every response. We weren’t getting anywhere with you repeating the same thing over and over again; and, since I’m very interested in getting somewhere with this discussion, I had to do something that might sound a bit condescending.I apologize for patronizing you, but how else could I have proven to you that I actually do understand your argument?

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.

Hi, Faith. I understand the feeling. I don’t have the stamina to hold up against even a few opponents, so I admire your fortitude.----- The way things are going now, I often feel like I’ll be dead by then, too. ----- Well, I didn’t: that figure was from a recently published study ( click here for a news article written about the study).In that study, the researchers actually sequenced the entire genomes of a husband and wife, and the genomes of their two children. They were able to identify places in the genome where the children’s sequence differed from both parents’ genomes. Each child’s genome contained about 70* places that differed from both parents’ genomes.That’s 70* differences (mutations) in one generation. *The news article says 60, but the actual study says 70 (I missed this on my first time through).----- The paper stated that both children had two recessive genetic disorders, but does not actually state whether these were due to mutation: my feeling is that these were not related to the mutations identified. As far as I can tell (most of the paper is beyond my education), none of the mutations identified was detrimental: given that the samples were taken from living children, the mutations were obviously at least not fatal.No data were presented on the phenotypic effects of the mutations, but, given that the children do not seem to have been adversely affected by any of these mutations, they would appear to be neutral or, at worst, very slightly deleterious, and some may even have been beneficial.----- There have been hundreds of scientific studies that have conclusively demonstrated that mutations happen. There is no way to realistically deny that mutations happen.Given that, we then have to decide what constitutes a beneficial mutation, and why this would represent a special case of a mutation that cannot happen.When we add to this the simple observation that the occurrence of mutations is not sensitive to the phenotypic effects that the mutation would have on the organism, I don’t see how there is anything that could stop a beneficial mutation from happening.In terms of the scientific method, the default conclusion is that beneficial mutations can and do happen. The alternative is to propose that there is a special mechanism in place that prevents mutations from happening if those mutations would have a positive effect on phenotype. Since there is no evidence for such a special mechanism, there is no reason to think that beneficial mutations are different from any other kind of mutation in terms of whether or not they can happen.It can be extremely difficult to identify beneficial mutations, because benefit is highly context-specific. For instance, mutations have been identified that cause plants to grow taller than they otherwise would. This would be beneficial where competing plants were tall, because it would allow the plant to reach sunlight, but it would not really be useful for a plant that has little competition for sunlight.However, many kinds of detrimental effects can be easily identified because of the obvious deformities they cause. This is the only really sure reason why we know so many more detrimental mutations than beneficial mutations.

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.

Hi, Faith.First off, you are overusing the word assumption: an assumption is something that cannot be based on anything. Since the idea of beneficial mutations is based on the observation that mutations occur, it is not an assumption.A hypothetical scenario is not even remotely similar to an assumption. Please stop flinging the word assumption around.----- Then you are asking for evolutionists to provide a level of proof that you would never ask of anybody else for any other claim!If I could prove to you that humans can walk, would you then demand additional evidence that shows that humans can walk to a water hole to get water? You would not demand this, because you know that the destination has no relevance whatsoever for the mechanism of getting there. If I can walk, I can walk to water. Period.But, in the case of mutations, you’ve totally flip-flopped your position, and are demanding that, after we have proven the proverbial ability to walk, we still have to prove the proverbial ability to walk to water.The functionality of the allele has absolutely nothing to do with whether or not the mutation that would create the allele can happen. So, if I can show you that a new allele can be produced (and I have done so), then I have shown you the ability to make a beneficial mutation. No assumptions are involved at all in this conclusion: every step of the process is supported by evidence. If a gene can change, it can change into something functional. Period.----- Once again, desirability has nothing to do with the mechanisms of allele production.
What part of that is so hard to understand?----- Okay, now you’re moving the goalposts. Why do I have to demonstrate that all alleles emerged this way? If I demonstrate that one alleles emerged this way (which I have done), I am vindicated, because it then falls on you to show that other alleles are somehow different from that allele.Besides, you’re reading everything we do in science backwards from the way it actually happens. Scientists started with the observation that mutations produce new alleles, and extrapolated that backwards to hypothesize that all alleles emerged this way. Since no one has produced evidence for any other mechanism by which alleles are generated, mutation is currently the only demonstrated way to explain the origin of alleles.Until somebody presents something better, this is what we have to work with to explain the genetic diversity of life. So, that’s what we use to construct our current model of life and its history. If you disagree with this model, the onus is on you to demonstrate that reality deviates from the model, not on us to provide better proof of what we have already demonstrated to be accurate.

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.

Hi, Faith.I’m as frustrated as you are: my points are also being ignored, misunderstood and misrepresented. But, from my perspective, it does not feel like you’re making a good-faith effort to understand what I’m saying to you. I have addressed your points, but my addressing them seemingly has no effect on how your next post is going to be composed.At any rate, your last post seemed like a lot of quasi-controlled ranting. You started talking about things that don’t make any sense at all (for instance, what is a normal allele?), and you seemed to have started thinking that alleles that cause deformities or other debilitations are not alleles, which is false and may have been a source of confusion about my arguments.I’m not going to respond directly to any comments you made, because I don’t think I have the maturity to handle that appropriately. Instead, I’m going to try to summarize the main thrust of my argument.I have been trying to get you to see that you are looking at this situation in an entirely inappropriate light. I have uncovered the two major points of contention that you have with the evolutionist argument, and I will now provide what I think are accurate rebuttals to those two points:

1. The difference between beneficial and deleterious mutations.
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   There is no difference between beneficial and deleterious mutations. At least, not for the molecules that cause them. At the molecular scale, a mutation is only a switch from an A to a T, or something akin to that. To the molecules, there is no beneficial or deleterious: they do not directly experience either one.
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   So, the monikers beneficial and deleterious do not apply to the mechanism of mutation. They only apply to the phenotype of the resulting allele. So, arguments about the mechanism of the mutation apply equally as well to mutations that would have a beneficial effect and to mutations that would have a deleterious effect. There is no mechanistic distinction between beneficial and deleterious mutations, so classifying them as "beneficial" and "deleterious" when discussing if and how they happen is meaningless: rather, we should be categorizing them mechanistically: i.e., "point mutations," "insertions," "deletions," etc.
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   This was where the walking analogy came in. Walking is walking. There is no mechanistic difference between walking to the store and walking to the park: in both cases, the same mechanism is used to get there.
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   Likewise for mutations. Mutations are mutations. There is no mechanistic difference between mutating into a beneficial allele and mutating into a deleterious allele: in both cases, the same mechanism is used to get there.
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   A beneficial mutation is just a specific case of a mutation, just as walking to the watering hole is just a specific case of walking. There's no reason to think it is somehow different from every other case of mutation/walking. That was the point of the analogy.
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   Do you understand what I’m saying?
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   For the record, I also feel like I am being made to cross all the t’s and dot all the i’s for you: you come off as an idiot to me as much as I come off as an idiot to you. We can solve this by (1) repeatedly libeling each other and calling each other idiots or (2) trying to understand each other in the hope that understanding will cure each other’s idiocy.
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2. What is based on what?
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   You think our argument unfolds as follows:
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   (1) Assume that all alleles come from mutations.
   (2) Observe an allele that we have never seen before.
   (3) Conclude that the allele came from mutation.
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   In actuality, our argument unfolds as follows:
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   (1) Demonstrate that mutations create new alleles.
   (2) Observe that no other means of creating alleles has been demonstrated.
   (3) Disregard these undemonstrated means of creating alleles.
   (4) Conclude that, to the best of our knowledge, all alleles come from mutations.
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   Then, only after that, we tack on two more steps:
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   (5) Observe an allele that we have never seen before.
   (6) Conclude that the allele came from mutation.
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   Your argument is that the first three steps never happened. This is simply false.
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   I’ll grant that some of us may get overzealous about our conclusion, and may not treat it with the proper air of tentativity, but it really is the only conclusion that can be arrived at by only using processes that have been demonstrated to happen. I don't see how logic could allow any other progression of thought on the subject.
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   The only remedy for this is to demonstrate that some other process that produces alleles is happening (e.g. an Intelligent Designer). In the absence of that, we literally have no choice but to fall back on mutation as the only possible explanation.
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   There is no sense in demanding that I prove that mutations could have caused situation X when it has already been shown that mutations have caused things that are mechanistically indistinguishable from situation X, and when nobody has been able to demonstrate that a suitable alternative explanation is viable.

-----I believe I have accurately represented your views here, and have provided solid rebuttals that should clear up your misgivings about the reasons we support mutation as the primary source of genetic diversity.I don't expect that this will change your mind about whether alleles arise by mutation, but I hope it will at least put an end to your inaccurate portrayals of our arguments and methods of reasoning.If you take these points under consideration, I think we're prepared to discuss the role of mutation in the processes of speciation and diversification.Edited by Bluejay, : "-----"

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-Bluejay (a.k.a. Mantis, Thylacosmilus)Darwin loves you.