Andre’s questions

Andre poses some interesting questions to Nick Matzke. I thought I’d start a thread that might help him find some answers.  I’ll have first go :

Hi Nick

Yes please can we get a textbook on Macro-evolution’s facts!

I’ll make it easy for you;

1.) I want to see a step by step process of the evolution of the lung system.

Google Scholar: evolution of the lung sarcopterygian

2.) Step by step process of the evolution of the heart.

Evolution of the Heart from Bacteria to Man

 

3.) Step by step process of the sexual reproductive system.

Well, there are rather a lot of sexual reproductive systems, but this might get Andre started:

Google Scholar: evolution of dioecy

4.) When did survival of the fittest kick in? With the first single cell organism or later? How did they know that survival is key?

This one just needs a little thought, rather than google.  “Survival of the fittest kick[s] in” as soon as you have any population of self-replicators that replicate with heritable variance in reproductive success in the current environment.  This is a matter of straightforward logic:

IF a population of self-replicators replicate with less-than perfect fidelity

AND IF some variants are better at self-replicating than others (tend to have more viable offpring)

THEN the variants that self-replicate better will become more prevalent.

This conclusion is sometimes referred to as the “survival of the fittest” (survival down the generations), and sometimes “natural selection”. So the answer to Andre’s question is this:  We do not yet know just how simple a self-replicator had to be in order to fulfil the two conditions necessary for Darwinian evolution (aka natural selection), but we do know that wherever those two conditions are present, Darwinian evolution will be the near-inevitable result. Current thinking is that the earliest Darwinian-capable self-replicators were probably a combination of self-replicating polymers enclosed in expandable and divisible lipid vesicles.

5.) How does natural selection select? If something is not in the search space how does it find stuff that is not there? Or has everything always been there?

Well “natural selection” is a figure of speech.  “Artificial selection” is selection of traits by artifice – by human breeders who desire particular traits in their livestock or plants.  So in “artificial” selection, the traits that promote successful reproduction are those that please the breeder, who then breeds from those individuals.  In nature the traits that promote successful reproduction are simply  those that facilitate breeding in the natural environment, hence Darwin’s use of the analogous term natural selection.

I think the “search space” metaphor has to be used with caution.  There is no Mother Nature who is “searching” for an ideal organism.  Rather, traits that best fit an organism to reproduce in a specific environment are the ones that become most prevalent in a persisting population. This is so obviously true that some people think it is tautologous.  It is not, but it is syllogistic.

However, if Andre’s question is about how the variants that confer those beneficial traits come about: I think there is a considerable misunderstanding about this.  Most traits are polygeneic, and the degree to which they are present or absent (e.g. spots; feathers; light-detection capacity) is governed by a whole host of DNA sequences, most of which regulate the process by which an infant becomes an adult, and each of which have many alleles.  So, for sexually reproducing species anyway, I think it’s misleading to think of specific variants as producing brand new traits – better to think of variance as a kind of constant drip-feed into the gene pool, most variants being neutral and propagating simply by drift; while “selection”  operates in any given environment by means of those organisms who inherit the most beneficial cocktail of variants spreading their particular inheritance more generously than those who inherit a less beneficial cocktail.  So in that sense, the “search” in every generation is simply for the optimum (in the current environment) allele set of those currently available.  Ten generations on, the set of possibilities will be slightly different, as will the current environment, so the population tends to “move” towards the distribution of alleles that works best of the options available.  It’s as though chocolate manufacturers kept on adding new chocolates to their boxes at whim, and removing others, and every so often, one particular selection takes the fancy of the customers (more truffles; fewer caramels) and suddenly the manufactureres of the boxes with lots of truffles and hardly any caramels experience much higher demand.  Thank goodness those green pralines have almost dropped out of the chocolate gene pool.

6.) If Random mutations are 90% bad most of the time why are we here? is 1% good enough to go from a single cell to a complex organism such as a human? Is this scientifically possible?

Mutations (whether you call them “random” or not depends on what you mean by “random” – most are probably the result of really quite highly deterministic processes, and certainly some kinds of mutations are far more probable than others) are not “90% bad most of the time”.  The vast majority are near-neutral.  However, in a poorly adapted population (perhaps one subject to rapid climate change) a larger percentage will tend to be beneficial than in a well-adapted population (one in a stable environment) so in the latter, more will tend to be “worse” than “better”.  And yes, a small percentage is enough – it’s not the percentage that matters, so much as the frequency of near-neutral mutations, and the rate of environmental change.

7.) How did the feathers evolve?

Lots of literature on this.  Try:

Google Scholar: evolution of feathers

8.) How did animals evolve from cold blooded to warm blooded?

Again, google scholar is your friend:

Google Scholar: evolution of thermal regulation warm-blooded

Your most valuable scientific facts will be greatly appreciated.

You are very welcome!

Good Luck!

Andre

And good luck with your searches 🙂  I’m sure some others will be along shortly to put me right/supplement your reading/explain more clearly.

Lizzie

28 thoughts on “Andre’s questions”

  1. damitall2

    Sorry, but my opinion is that if anyone really wanted to know if there were even partial answers to these questions, he/she would have the gumption to do a little research for him/herself.

    With Google Scholar and the rest of the internet at one’s fingertips, there is no excuse for not doing it.(Assuming the questioner Really Wants To Know)

    Requests for clarification of knotty points – fine. Arguments about interpretation of data – fine.

    The sort of attempted triumphalism we’re treated to by “Andre” -idiotic

  2. Lizzie

    Well, yes, but it was sort of fun. I mean what do they think that scientists actually do? And if evolutionary theory was as patently idiotic as some of the ID proponents seem to think, do they really think someone wouldn’t have noticed?

  3. Joe FelsensteinJoe Felsenstein

    For the question about mutations being “90% bad most of time” and “1% good”: I am not sure what assertion that is (I notice that 0.90+0.01 is not 1.00), but even if 99% of all mutations are deleterious and 1% are advantageous, the result can be more advantageous changes than deleterious ones. Creationists concerned about this (and it is a big concern mostly of YEC creationists) don’t actually sit down and do the math, using Kimura’s 1962 probabilities of fixation of new mutants.

    If they did, they would find out that in a population of (say) 1,000,000 diploid individuals, a mutant allele with a 1% higher fitness will fix 0.0198 of the time. But a mutant with a 1% lower fitness will fix only one out of 10-to-the-17372 times. In other words, never once in the history of the universe.

    So just noting that more deleterious mutants arise than advantageous ones is not enough to understand the net outcome,

  4. damitall2

    Lizzie,

    I know, I know.
    I’m grumpy today.

    Anyway, discussing science with ignorami is only sometimes fun. Usually it’s a waste of time and electrons

  5. Lizzie

    Can you explain something to me, Joe? I’ve always been puzzled why “fixation” is an important marker- it always seem to me that the opposite – when a new, or old, allele drops out of the population – is a more salient event. I mean, how many alleles are ever actually “fixed”?

  6. sholom

    I think that they think the scientists are well aware of the idiocy of evolutionary theory. But their atheism/materialism prevents them from being honest about it.

  7. Lizzie

    sholom:
    I think that they think the scientists are well aware of the idiocy of evolutionary theory.But their atheism/materialism prevents them from being honest about it.

    What makes you think this?

    After all, a great many scientists are not atheists.

  8. Lizzie

    I think one of the problems is that people who are anti-evolution for whatever reason think that biologists are claiming to have all the answers. Clearly this is not the case, and nor is it the claim they make.

    One of the assymmetries between the ID position and the mainstream scientific position is that ID proponents claim, positively, that the data suggests an ID, as an explanation for what mainstream science cannot yet explain in detail (presumably that lies behind Andre’s request for detailed accounts of the evolution of various features). In contrast, mainstream scientists merely claim that while much remains – and will always remain – unexplained, we do not have cause, yet, at least, to seek explanations that involve volitional agencies not otherwise in evidence. Scientists do NOT conclude that only “material” agencies were involved, at least qua scientists, although some may do so qua people-with-a-hunch. Methodologically, science simply does not equip us with the tools to draw such a conclusion.

  9. Zachriel

    Lizzie: I’ve always been puzzled why “fixation” is an important marker- it always seem to me that the opposite – when a new, or old, allele drops out of the population – is a more salient event.I mean, how many alleles are ever actually “fixed”?

    Fixation and extinction of alleles are interesting theoretical problems, but in real life, most variations are nearly neutral.

    The simplistic model is a uniform population. Everyone is a clone of Lizzie, except for the occasional Lizzie with a mutation that is most probably deleterious. Even if the mutation is somewhat advantageous, it may take a multitude of generations for it to become fixed in the uniform population, if ever. Now, compare that to the real world of human organisms, with billions of highly distinct individuals, most of whom are reasonably adapted to their environment, yet each a unique mix of traits—a cacophony of variations, not a monotone.

  10. Joe FelsensteinJoe Felsenstein

    Lizzie,

    In these simple selection models most mutations to even an advantageous allele get lost, and very rapidly. If the allele has selective advantage of (say) 0.01 you can show that it will rise to fixation, with little chance of being lost, if it ever makes it up to (say) 200 copies in the population, which is still a very low frequency,

    So there’s not much difference, in such a model between calculating the probability of getting into the population and calculating the probability of ultimate fixation.

    [Woops, posting mistake — this is an answer to Lizzie’s question several comments earlier]

  11. Lizzie

    One thing that has really struck me recently is the disappointingly (at first sight) feeble results from GWAS. We know that certain disorders like schizophrenia and ADHD are highly heritable (estimates well over 50% heritability) and yet any one SNP with a statistically significant association has an odds ratio of little over 1 – in other words the vast majority of people with the “risk” allele are absolutely fine.

    This seems to me to be powerful confirmation of the idea that phenotype traits are so polygeneic, that the Central Limit Theorem applies, and the tails are marked by very low-frequency alleles of a wide assortment of genes, rather than specific alleles of a few. That’s why I find it more constructive to think in terms of a constant drip-feed of near-neutral variance into the gene pool, which the environment filters with a fairly generous roll-off, to increase the prevalence of those most often associated with reproductive success in the current environment, even though most of those “selected” will have been around for ages before turning out a little bit handy. In fact, I wonder whether it is really very rare for any single new allele to be immediately beneficial. My guess is most are “bought for stock” as it were. Or rather, just retained for no very good reason, rather like the contents of my garage. And chucked out for no terribly good reason either.

    After all you never know when that manky old bit of bungee cord, or that Australian electrical socket might come in handy, although too often it does just when you finally took it to the tip.

  12. Lizzie

    Joe Felsenstein:
    Lizzie,

    In these simple selection models most mutations to even an advantageous allele get lost, and very rapidly. If the allele has selective advantage of (say) 0.01 you can show that it will rise to fixation, with little chance of being lost, if it ever makes it up to (say) 200 copies inthe population, which is still a very low frequency,

    So there’s not much difference, in such a model between calculating the probability of getting into the population and calculating the probability of ultimate fixation.

    [Woops, posting mistake — this is an answer to Lizzie’s question several comments earlier]

    Thanks! Yes, that was sort of my understanding, based mostly on messing about with evolutionary models.

  13. Joe FelsensteinJoe Felsenstein

    There is an active debate among genomicists as to whether the genetic variability that accounts for the “missing” heritability is rare alleles maintained by mutation, or more common alleles that are of small effect. Each side maintains that their view is the well-supported consensus and that the folks on the other side have no one supporting them.

  14. Allan Miller

    Can you explain something to me, Joe? I’ve always been puzzled why “fixation” is an important marker- it always seem to me that the opposite – when a new, or old, allele drops out of the population – is a more salient event. I mean, how many alleles are ever actually “fixed”?

    Can I take a stab? If you mean without subsequent mutation, very infrequently. One could get a firmer idea by the extent of polymorphism across the genome. All invariant sequences are (or rather have become) fixed.

    But one can look at alleles simply as descendant sequences, coalescing upon different members of an ancestral population, and their fixation is almost inevitable (assuming no extinction or internal recombination). Alleles designated by descent do not necessarily map fully upon sequences differentiated by their content, due to further mutation.

    Because frequencies always add up to 100%, fixation and extinction are two sides of the same coin. The point when allele A drops out of the population is also the point at which not-A becomes fixed. One could argue that an allele has become part of the ‘consensus genome’ when it has passed 50%. But there remains a nonzero probability that, even when down to its last representative, the rival could re-emerge and recolonise its locus (this is, after all, how new mutations become the norm, by starting from a single instance). So fixation (ie: extinction) is the point at which that becomes no longer possible.

  15. Lizzie

    Joe Felsenstein:
    There is an active debate among genomicists as to whether the genetic variability that accounts for the “missing” heritability is rare alleles maintained by mutation, or more common alleles that are of small effect. Each side maintains that their view is the well-supported consensus and that the folks on the other side have no one supporting them.

    Yes, I’ve been to such debates 😉

  16. damitall2

    Lizzie: Yes, I’ve been to such debates

    What?!

    You mean scientists are skeptical about each others’ results?

    Better rush to tell Barry Arrington and Kairosfocus – they seem to think this never happens

  17. Lizzie

    Allan Miller: But one can look at alleles simply as descendant sequences, coalescing upon different members of an ancestral population, and their fixation is almost inevitable (assuming no extinction or internal recombination). Alleles designated by descent do not necessarily map fully upon sequences differentiated by their content, due to further mutation.

    OK, thanks, that makes sense!

  18. Lizzie

    damitall2: What?!

    You mean scientists are skeptical about each others’ results?

    Better rush to tell Barry Arrington and Kairosfocus – they seem to think this never happens

    Barry and KF (and others) are stuck in a closed loop, whereby disagreement between scientists supports the idea that the consensus is crumbling, and while agreement supports the idea that scientists are terrified to dissent from “the Academy”.

    It’s like (well, it is) conspiracy theory, whereby apparently discrepant data show there is a problem, while innocent explanations for the discrepant data shows there is a cover-up.

    That’s not to say that scientists are never wrong, or even biased, or that there are no conspiracies. Scientists are often wrong and biased, and there are indeed conspiracies.

    The problem is that once you get into a closed loop whereby all possible revelations are confirmatory, you have no way of testing your own take. Once you doubt the ability of the science as an institution to be self-correcting, you have no option but to figure out everything for yourself, which no one person can do. Or to put your trust in people who seem to share your “worldview”, and who seem to know what they are talking about.

    Even when they patently don’t.

  19. Allan Miller

    OK, thanks, that makes sense!

    Rereading – not so much! By ‘inevitable fixation’ (as you probably realised) I didn’t mean they would all fix inevitably … ! But it is one of the interesting things about the kind of sampling-with-replacement that goes on in finite populations that the only way to oppose fixation (of one ancestor or another, irrespective of any selective differential) is to have a selective process favouring underdogs.

  20. Zachriel

    Joe Felsenstein: So there’s not much difference, in such a model between calculating the probability of getting into the population and calculating the probability of ultimate fixation.

    Then, the significant factor is time to fixation. A recessive trait, or a nearly neutral trait, may persist for a very long time in a large population before extinction or fixation. The result is the huge amount of variety that can co-exist within populations, so much so that nearly every individual is unique.

  21. Flint

    It’s a syllogism:
    1) Evolution is false. It doesn’t happen. Period.
    2) Many scientist act like they don’t realize this
    3) Therefore, either they are dishonest or deluded.

  22. petrushka

    More interesting to me is the possibility that each neutral variation represents a possible branching point, because it could be an enabling mutation.

  23. damitall2

    Now that Andre has (no doubt) taken up and read the references given by LIzzie in her answer to his questions, perhaps he, or one of his buddies will give us the answer to this question – which has been asked many, many times before, but never yet answered…

    Can you suggest a plausible mechanism by which any disembodied designer could push atoms and molecules around into his/her/its desired combinations and configurations?

    “We” have the laws of chemistry and physics (agreed to exist) , coupled with heritable variations (observed and agreed to exist) and natural selection (observed and agreed to exist); and we have some evidence to show that these can account for the diversity of life.

    Can Andre or any IDist come up with similarly plausible, but different, mechanisms?

    Or, leaving aside the question of the Origins of Life (which none of us know, but at least some of us are working on) can they show any evidence that the potential for specified diversity was somehow “built in “; and/or that subsequent variations are/were “directed”?

    Or is it possible that they can be honest and admit that these would be unsupported assertions?

  24. Zachriel

    petrushka: More interesting to me is the possibility that each neutral variation represents a possible branching point, because it could be an enabling mutation.

    Sure. With large populations replete with variations, that’s possibly billions of branching points, with all sorts of synergies available between traits.

    IDers often think in terms of a simplistic model, rather than the richness of real life.

  25. Lizzie

    Zachriel: Sure. With large populations replete with variations, that’s possibly billions of branching points, with all sorts of synergies available between traits.

    IDers often think in terms of a simplistic model, rather than the richness of real life.

    Indeed. I think this is the core of the problem. Or one of many worms at the core of the problem: taking a limited model e.g. two dimensional fitness landscapes or coins with two faces, or traits with two alleles, then scaling it up linearly to conclude that the modelled thing must be similarly limited

    Nonlinearity is off the agenda, it seems, as is the idea that when scaled up, factors that were discrete become, essentially continua, as do heritable traits.

    The propagation of specific alleles through a population is to natural selection as brownian motion is to pressure differentials.

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