445 thoughts on “Evolution Visualized”

  1. Petrushka:

    It looks to me like mutations per base pair is similar in all cellular organisms

    Yes, but things like the Muller limit deal with mutations per individual not per base pair. E coli has a smallish genome (50 mega bases), humans have 3.3 giga bases. Therefore humans, if the genomes are mostly functional have over sixty times the number of mutations per individual.

  2. petrushka, that sounds right. But we have a lot more DNA than microbes. Among the microbes that do have huge genomes, the large majority of it is likely either redundant failsafes or it’s junk.

  3. JoeCoder: petrushka, that sounds right. But we have a lot more DNA than microbes. Among the microbes that do have huge genomes, the large majority of it is likely either redundant failsafes or it’s junk.

    But not many bacteria have a lot of junk.

    I guess the questions I have are: are you adjusting for the fact that only two percent of human DNA codes for protein (and is under heavy selection pressure) and the remaining functional DNA is subject to less selection because, well it just isn’t as critical.

    I don’t get any sense that MA has a clue as to what it means in biology to be detrimental or neutral. It’s just abstract numbers, whereas in real life, traits have complex effects.

  4. are you adjusting for the fact that only two percent of human DNA codes for protein (and is under heavy selection pressure) and the remaining functional DNA is subject to less selection because, well it just isn’t as critical.

    Yes. When we say things like u=10 or u=20 we are assuming that 10 or 20% of the genome is subject to deleterious mutations. I expect more of it than this is but I am sticking with these values because I think they are easily defensible. For my defense of u=20 see my first comment on page 3 of the comments.

    By default Mendel uses a continuous probability distribution to assign the effect of deleterious mutations, with a small number being highly deleterious and more mutations being slightly deleterious.

  5. JoeCoder: By default Mendel uses a continuous probability distribution to assign the effect of deleterious mutations, with a small number being highly deleterious and more mutations being slightly deleterious.

    Since I think physics has the age of the earth right, and I see no interesting evidence against common descent, I look at assertions being made by the MA proponents and say, you need to figure out why your program doesn’t comport with reality.

    I notice that Behe uses something akin to your line of reasoning the The Edge. He seems to take an arbitrary definition of detrimental and argue that evolution can’t maneuver around detrimental mutations. Reality seems to argue otherwise.

    I don’t expect to settle this here, but I’ve been following this debate since 1956, and have seen a steady retreat from creationist claims.

    Assuming your arithmetic is correct, I would bet your model has some important gaps.

  6. JoeCoder,

    I understand the code, but I didn’t have it in front of me when I wrote that comment and I mis-remembered what number mapped to what mode.

    There’s a lesson there.

    Selection scheme 1 is the one that uses strict truncation selection.

    All four schemes use truncation selection, regardless of their names. The only difference is in whether, or how, they scale and randomize the phenotypic fitnesses before applying the truncation selection.

    This is important, because it shows that reproductive success is proportional neither to fitness nor to fitness ranking. Those two statements you quoted earlier are not only contradictory — they’re both wrong!

  7. keiths: This is important, because it shows that reproductive success is proportional neither to fitness nor to fitness ranking. Those two statements you quoted earlier are not only contradictory — they’re both wrong!

    I think I’ll come back to this and I hope to find a clear and complete summary. Maybe in an OP. It is obvious to me that the model doesn’t reflect reality, but my math skills are inadequate to see where the problems lie.

  8. Petrushka, why do you think the Mendel results are incompatible with old earth creation or theistic evolution? This is the third time you’ve made this claim and I’ve addressed it twice.

    Behe seems to take an arbitrary definition of detrimental and argue that evolution can’t maneuver around detrimental mutations

    It’s been a long time since I’ve read Edge. But if I remember, the argument is that if you need two simultaneous mutations to get a feature, and the intermediate is deleterious, then the odds of this happening are the square of the mutation rate.

    Larry Moran seems to agree with this part: “The probability of any single mutation occurring is equal to the mutation rare, which is about 10^-10. The probability of an additional specific mutation occurring is also 10^-10. The combined probability of any two specific mutations occurring is 10^-20.”

    What is the example to the contrary? But this has nothing to do with any of the deleterious load arguments we are having here.

    I’ve been following this debate since 1956, and have seen a steady retreat from creationist claims.

    I see the opposite trend. We’re still using the same population genetics formulas, but the functional genome size has exploded since then.

  9. kieths, you write:

    All four schemes use truncation selection, regardless of their names.

    Then we’re not talking about the same thing when we say “truncation selection.” Wikipedia defines it: “In truncation selection the candidate solutions are ordered by fitness, and some proportion, p, (e.g. p = 1/2, 1/3, etc.), of the fittest individuals are selected and reproduced 1/p times.”

    Only selection_scheme==1 does this. The other modes incorporate a randomness to their order so that its not strictly ordered by fitness, but those that are more fit are still more likely to survive than those that are less fit.

    it shows that reproductive success is proportional neither to fitness nor to fitness ranking.

    kieths, In all four schemes, those that are more fit are more likely to survive than those that are less fit. Even in unrestricted probability selection, selection is stronger than it should be according to my Barney Fife and Genghis Khan reproduction. Or it’s possible I’m in error, since stcordova says Mendel matches the equations of Kimura.

  10. JoeCoder: Petrushka, why do you think the Mendel results are incompatible with an old earth or common descent?

    Tell me how common descent is compatible with MA.
    Tell me a story about the history of life as you think it happened.

  11. Petrushka:

    But not many bacteria have a lot of junk.

    Only 20% of E. coli genomes are conserved. They do seem quite tolerant of change, and most the changes are in the coding region (like wholesale gene deletions) since bacteria don’t have a lot of non-coding regions (compared to humans).

    The human genome may be much more sensitive to change, it is 99.5% conserved, so that’s a lot more than E. coli. The human genome has lots of binding motifs that overlap exons, miRNAs that regulate enforce highly specific codon biases. Who knows what else. The human genome may be substantially more fragile than bacterial genomes.

  12. Petrushka, check out page 4 of the comments, comment number 34. You even responded to that comment so I know you saw it 🙂

  13. stcordova:
    . . .
    So can we provide documentation for Mendel’s Accountant?Probably not.

    You don’t need Mendel to be documented to build your own pop gen software.
    . . . .

    We do need clear documentation of the model in order to assess the claims being made about the software that implements it.

  14. JoeCoder: So what does that mean theologically? Some take this and argue for young earth creation, as Sanford does. Or you could say God interferes to drive and correct evolution, as theistic evolutionists do. Or maybe God continually replants the orchard, as the old earth creationists assume.

    It’s magic sky fairy stuff. Good luck with that.

  15. Yes, those sorts of interpretations of the data are ridiculous. I just wish there could be some agreement on the data. There shouldn’t be any need even for somewhat more sensible interpretations.

  16. Trying to go on a low snark diet.

    Science can’t prove that angels aren’t tweaking genomes, and ID can’t prove that it’s analysis hasn’t overlooked a natural cause.

    I can only ask, considering the last 300 years of science, which conjecture has been more productive.

  17. Patrick: What is the exact model that MA is implementing, in enough detail to allow an alternative implementation to be created? This is followed immediately by: What real world observations support the results of that model?

    What exact model did the keiths drift weasel implement and what real world observations support the results of that model?

    Not sure why this is only an issue for you now.

  18. stcordova: But this would all be moot if the Mendel detractors provided the software suite of their choice to model these issues.

    I bet Joe F. has some.

  21. Patrick: We do need clear documentation of the model in order to assess the claims being made about the software that implements it.

    What model does Weasel implement?

    Do you have any evidence from biology to support that claim?

    What real world observations support the results of that model?

  22. Mung: What model does Weasel implement?

    As pointed out in my thread on Wright, Fisher, and the Weasel, the Weasel comes close to a Wright-Fisher model with one haploid adult surviving every generation, provided the number of offspring each generation is made suitably large.

    Do you have any evidence from biology to support that claim?

    The claim that the Weasel comes close to the WF model is supported by analysis of both models and by the similarity of results when they are run.

    Or was Mung asking for evidence from biology to support the assertion that the Weasel is a realistic model of real population? If so, what a silly thing to ask for — no one has argued that Weasel is a realistic model of a real population.

    What real world observations support the results of that model?

    Again, what a silly thing to ask for! The Weasel is designed (yes, designed) to be an analyzable model of a process of cumulative selection. Which Mung has acknowledged that it is.

  23. Joe Felsenstein: If so, what a silly thing to ask for — no one has argued that Weasel is a realistic model of a real population.

    It seems important, all of a sudden, when examining creationist claims. And that’s what Weasel was intended to do, according to you.

  24. keiths:

    All four schemes use truncation selection, regardless of their names.

    JoeCoder:

    Then we’re not talking about the same thing when we say “truncation selection.” Wikipedia defines it: “In truncation selection the candidate solutions are ordered by fitness, and some proportion, p, (e.g. p = 1/2, 1/3, etc.), of the fittest individuals are selected and reproduced 1/p times.”

    Only selection_scheme==1 does this. The other modes incorporate a randomness to their order so that its not strictly ordered by fitness, but those that are more fit are still more likely to survive than those that are less fit.

    In all four schemes, offspring are sorted by fitness — the specific variable is called ‘work_fitness’ — and the least fit individuals are truncated. The differences among the schemes lie in how work_fitness is generated.

    In scheme 1, phenotypic fitness is assigned directly to work_fitness. In the other three schemes, phenotypic fitness is modified in a way that depends on a random variable before it is assigned to work_fitness.

    In all four schemes, truncation selection is applied. That is, the organisms are sorted by work_fitness and the least fit organisms get the axe.

    The Mendel code is unambiguous:
    if (selection_scheme <= 4) {

    /* Apply truncation selection to reduce the population size to
    current_pop_size. */

    If you want to argue that the Mendel authors didn’t understand truncation selection, despite using it, then be my guest. It doesn’t help your case.

    keiths:

    All four schemes use truncation selection, regardless of their names. The only difference is in whether, or how, they scale and randomize the phenotypic fitnesses before applying the truncation selection.

    This is important, because it shows that reproductive success is proportional neither to fitness nor to fitness ranking. Those two statements you quoted earlier are not only contradictory — they’re both wrong!

    JoeCoder:

    kieths, In all four schemes, those that are more fit are more likely to survive than those that are less fit.

    Do you know what the word “proportional” means?

  25. stcordova: Yes, but things like the Muller limit deal with mutations per individual not per base pair.E coli has a smallish genome (50 mega bases), humans have 3.3 giga bases.Therefore humans, if the genomes are mostly functional have over sixty times the number of mutations per individual.

    I guess you wanted to write 5 instead of 50, because you get the relative fraction right, but the E coli genome is more like 4.5 megabases, not 50.

    I just discovered there’s a microbe wiki 🙂

  26. JoeCoder: Among the microbes that do have huge genomes, the large majority of it is likely either redundant failsafes or it’s junk.

    I’m sorry but no, that redundant failsafe stuff has zero evidence that it correlates with genome size. And with respect to bacteria, it is generally understood that they have pretty much zero junk DNA.

  27. stcordova: Petrushka:

    But not many bacteria have a lot of junk.

    Only 20% of E. coli genomes are conserved.

    Compared to what? Other E coli? To what degree are they conserved?

    They do seem quite tolerant of change, and most the changes are in the coding region (like wholesale gene deletions) since bacteria don’t have a lot of non-coding regions (compared to humans).

    Yes, but most of this owes to the fact that the general trend of adaptation in a static environment with a few basic nutrients supplied in the same form, is genome reduction because replication speed overshadows everything else. That wouldn’t really be true in your gut.

    In a typical minimal medium, you give a bacterium maybe 7 compounds and some minerals and keep it at the same temperature and atmosphere. The barest minimum to survive and grow, hence the name.

    There’s a far cry from saying many of the genes in a given E coli cell from your gut are useless in a synthetic growth-flask with minimal medium kept at constant temperature and atmosphere, and as such can be shedded without any cost in terms of viability, to saying large parts of the E coli genome in general, is junk.

    These shedded genes are important in a complex and constantly changing environment (that can move up and down a scale in terms of pH, occasionally surrounded by digestive enzymes, amount of fluid, coexisting with many other species of bacteria and so on ) where the organism is constantly under selection to keep a large repertoire of metabolic and regulatory genes so it can readily digest literally tens of thousands of different compounds the food you eat migh contain.

    It’s really not that odd they can shed large amounts of genes in such a state. I wouldn’t want my gastrointestinal E coli population replaced with Lenski’s experimental populations.

    The human genome may be much more sensitive to change, it is 99.5% conserved,

    What proportion of it? Over what timescales? Compared to what?

    so that’s a lot more than E. coli. The human genome has lots of binding motifs that overlap exons, miRNAs that regulate enforce highly specific codon biases. Who knows what else. The human genome may be substantially more fragile than bacterial genomes.

    For the reasons stated you can’t draw this conclusion from the evidence you mention.

  28. petrushka: Wouldn’t it be simpler just to exclude that portion of the genome which is known to be insensitive to mutations? At least as a reasonable approximation.

    No, my question was a sort of test of the program. If it predicts meltdown for a 20% functional human genome, how much would have to be junk for no meltdown to happen? 10%? 5%? That’s what I want to know.

    petrushka: And does MA treat protein coding and regulation as equally sensitive to mutation? Equally subject to purifying selection?

    As a population-genetics simulator it is too abstract to consider things like regulatory vs coding regions. It just makes certain basic assumptions about the fitness effects of mutations if averaged across the whole genome. Some proportion are deleterious, a lesser portion is neutral, and the smallest is beneficial. It seems to me the key variables then are reproductive rate, population size and the selection coefficient distributions of beneficial and deleterious mutations.

    How deleterious is the average deleterious mutations? How beneficial is the average beneficial mutation?

  29. JoeCoder: If that’s their goal they’re doing a very lousy job at it. If probability selection divided by randnum^2 as it should, then selection in Mendel would be even weaker and deleterious mutations would accumulate even faster.

    Why? Would that not equally affect both deleterious and beneficial mutations?

    If there’s an overall strength of selection that artifically inflates the fitness values associated with certain mutations, then it seems to me it would affect both beneficial and deleterious mutations.

    For example, if 80% of mutations are deleterious with a selection coefficient of s = -0.02, and 1% are beneficial with average s = +0.02, and there’s an artificial inflation of the selection coefficients to s = -0.04 and s = +0.04 respectively, wouldn’t that give the same net result in terms of the speed at which meltdown occurs?

  30. stcordova: Thanks for your response, but I didn’t not describe the problem as well as I could, and had read references about the J family even better than the ones you provided..So let me restate the issue.

    There is divergence in the J family such that if the molecular clock hypothesis is correct, it indicates the J family is about 44 million years old by looking at the sequence divergence in the family members residing in the genome of humans. I depict the graph showing this and the 11% divergence within the same genome (intra species).

    The problem however is that this divergence is measured within the Alus in the same genome. If we do interspecies divergence however, we may come up with a paradox.

    If the same J family members appear in each primate line long after their supposed split, this would require convergent evolution of mutations in the corresponding Alus in the same genomic locations in the other primate lines.

    Yes. So IS there convergent evolution in the ALU substitutions and to what extend?

    How convergent are they? If looking at the genome overall, does it significantly deviate from the degree of convergence you might expect to some times happen by chance?

    The problem is analogous to the problem of SINES in rats and rhodents that Sternberg reported on:
    http://theskepticalzone.com/wp/some-evidence-alus-and-sines-arent-junk-and-garbologists-are-wrong/comment-page-3/#comment-139496

    Well, I think the analogy is quite inexact here. There’s a significant difference between the stochastic accumulation of substitutions and the method by which ALU’s insert themselves. On the face of it I’d suspect ALU’s in general are prone to finding roughly similar looking sites and insert themselves.

    Did the same point mutations simultaneously appear in J-Alus within gibbons and humans in the same genomic locations long after the supposed split.

    I don’t know, you tell me? Did they? How many? Of the proportion of overall genomic substitutions, is it a massive statistical deviation or would we expect such convergences to occasionally happen by chance?

    You haven’t brought any evidence here, so it looks to me like you’re inventing a problem nobody has even shown to exist. Are you anticipating this to be turn out ot be a problem or are you complaining that nobody has investigated the similarities in substitutions in the Alu J family in multiple primates to see if there’s convergence and how much?

    From here it looks like you ‘re basically just saying “there might be a problem here, but I actually don’t know and I don’t even know if it’s at all likely that there is, but noone’s looking at it as far as I know”. Well fuck me.

    If the same Alu J family members are in the same genomic locations in other primates long after their split, this means that somehow magically the Alu J members mutated the same way in each of the primate lineages.

    No, you are conflating insertion position of ALU’s as they proliferate in number, with the individual substitutions that happen IN those ALU’s. These two things are not the same.

    That’s the problem that should be looked at.

    Should it? It looks like a complete red herring to me. I can think of a million much more interesting evolutionary questions to investigate than that one.

    I don’t get the feeling anyone really wants to probe this question.

    You know what? I think you’re right.

    And even if the J families in other primates are different but at the same genomic locations, it results in the same problem that Sternberg found for the SINEs for rats and mice.

    Could ALU insertion locations be non-random or have a heavy stochastic bias towards certain locations according to their properties? Would this be a novel phenomenon that reveals a deep evolutionary conondrum? Yes and no, respectively.

  31. stcordova: But this would all be moot if the Mendel detractors provided the software suite of their choice to model these issues.

    Sure, but if a model is shown to contradict the real world, then the model very well can’t be used to falsify the real world, it’s the other way around.

    The absense of an accurate model is not evidence that reality is false. If there’s no alternative to MA, but MA cannot reproduce experimental results, then the solution isn’t to just blindly accept what MA says. You go by your experiment and make another model instead.

    JoeCoder seems to suggest the reason real populations don’t melt down is because god is intervening at the mutational level. In other words, that MA is right about what SHOULD happen if population genetics is correctly describing the evolutionary process, but in the real world God internvenes. Which would be funny if it wasn’t so ridiculous.
    It seems simpler to me to just say MA is probably not correct. Or that, and this is probably a long shot, it might even be the case that our best population genetics isn’t an accurate reflection of reality too and needs revision.

    Hey, aren’t creationists all for the “3rd new way” of evolution?

  32. Rumraket: JoeCoder seems to suggest the reason real populations don’t melt down is because god is intervening at the mutational level. In other words, that MA is right about what SHOULD happen if population genetics is correctly describing the evolutionary process, but in the real world God internvenes. Which would be funny if it wasn’t so ridiculous.
    It seems simpler to me to just say MA is probably not correct. Or that, and this is probably a long shot, it might even be the case that our best population genetics isn’t an accurate reflection of reality too and needs revision.

    Hey, aren’t creationists all for the “3rd new way” of evolution?

    I think you’re right that IDer’s conclusions don’t follow, but they’re really about a burden claim here, aren’t they? I mean, you’re right that what’s going on in the world is going on–no computer model can contradict THAT. But that’s not their goal, I don’t think. Rather, it’s simply the claim that what is incontestably going on isn’t the sort of thing that nature could do ON ITS OWN. It’s contrary to any combinations of statistical randomness and selectivity by fitness levels that can be (or at least has so far been) concocted. My own sense is that that claim simply must be wrong, that smart people plus computers could put together a reasonably representative model. But I recognize that the natural world is incredibly complex, and, in addition (as must have long been clear to people here), I have very little idea what I’m talking about in this arena.

    (I really wish Allan Miller would write his book already!)

  33. Forward-time population genetic simulation is not exactly an area of research whose literature I’m up to speed on, but here are a few additional programs (found via Google Scholar) that might be of interest:

    – simuPOP ( Peng and Kimmel 2005)
    – EasyPop (Balloux 2001)
    – ForSim (Lambert et al. 2008)
    – AnA-FiTS (Aberer & Stamatakis 2013) Stamatakis is also the guy who created the widely-used maximum Likelihood phylogenetic program RAxML
    – FORWSIM (Padhukasahasram et al. 2008)
    – SFS_ CODE (Hernandez 2008)
    – Genomepop (Carvajal-Rodríguez 2008)
    – Nemo (Guillaume and Rougemont 2006)
    – metasim (Strand 2002)

  34. I think that the MA crew is operating under the theory that the world, or at least the human population, is deteriorating since a point about 6000 years ago, and The End Is Nigh. Thus they are not trying to see what evolutionary forces enable populations to survive.

  36. Joe Felsenstein:
    I think that the MA crew is operating under the theory that the world, or at least the human population, is deteriorating since a point about 6000 years ago, and The End Is Nigh.Thus they are not trying to see what evolutionary forces enable populations to survive.

    The possible election of Donald Trump leads me to similar conclusions.

  37. I said:

    Only 20% of E. coli genomes are conserved.

    Rumraket asked in response:

    Compared to what? Other E coli? To what degree are they conserved?

    Here is the paper I got the figure from, maybe it can answer your questions, maybe not, but this is my source (plus the relevant quote below):
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2974192/

    It is a sobering thought to realize that any given E. coli genome sequenced will have only roughly 20% of its genes part of the E. coli core, and the remaining 80% are not found in all other E. coli genomes.

  38. Mung:

    What is the exact model that MA is implementing, in enough detail to allow an alternative implementation to be created? This is followed immediately by: What real world observations support the results of that model?

    What exact model did the keiths drift weasel implement and what real world observations support the results of that model?

    Not sure why this is only an issue for you now.

    False equivalence. The supporters of MA are claiming it reflects reality. In order to determine if that is the case, the model it implements must be clearly defined and any evidence for the claim must be provided.

  39. Rumraket:

    it might even be the case that our best population genetics isn’t an accurate reflection of reality too and needs revision.

    Pop gen good for modeling some things, but to the extent relative fitness of traits(described by the S-coefficients) is ever changing in real populations and it’s properties completely unknown (especially for near neutral traits), pop gen will come up with some un-useful results.

    This is really obvious in the case of reductive evolution. Koonin pointed out reductive evolution is a dominant mode of evolution. The paper is here:

    https://www.ncbi.nlm.nih.gov/pubmed/23801028
    A common belief is that evolution generally proceeds towards greater complexity at both the organismal and the genomic level, numerous examples of reductive evolution of parasites and symbionts notwithstanding. However, recent evolutionary reconstructions challenge this notion. Two notable examples are the reconstruction of the complex archaeal ancestor and the intron-rich ancestor of eukaryotes. In both cases, evolution in most of the lineages was apparently dominated by extensive loss of genes and introns, respectively. These and many other cases of reductive evolution are consistent with a general model composed of two distinct evolutionary phases: the short, explosive, innovation phase that leads to an abrupt increase in genome complexity, followed by a much longer reductive phase, which encompasses either a neutral ratchet of genetic material loss or adaptive genome streamlining. Quantitatively, the evolution of genomes appears to be dominated by reduction and simplification, punctuated by episodes of complexification.

    So, in a reductive scenario where an entire gene locus is lost in the species, what happens to the Allele’s of that locus and the associated S-coefficients (relative fitness scores) of those alleles? Gone! If there was a loss of function in this process whereby the loss of function was fixed into the population (I hate that word usage of “fixed” since it suggests “fixed” as in repaired, but it means “this broken feature is now in every individual”), the functional defect that is now present in every individual is no longer accounted for, just erase off the books as if there was never a problem.

    In pop gen mathematical models this issue is swept over by a mathematical accounting trick which says the population is always becoming better adapted (whatever that means) even though entire genes are being removed!

    But I don’t reject all pop gen. Some of the math of pop gen is relevant and there is no better example than the work of Muller who was very concerned with genetic deterioration. Muller won the Nobel Prize for study of radiation effects on the genome, and I suspect the question of how much the human genome can tolerate damage was often present in Muller’s mind. The figure of 1 bad mutation per generation as the Muller limit seems correct to me and many others. Since the S-coefficients are so ambiguous and changing at each nucleotide position, I tend to ignore them. S-coefficients relate to reproductive success which although occasionally correlated with functional health, reproductive success is most certainly not the same thing as medically healthy. “Fit” in the medical sense is certainly not “fit” in the pop gen sense.

    The Muller limit is logical and straight forward, furthermore it is experimentally testable. If we see that each subsequent generation on average has small functional defects than the prior generation, then we know we’re past the Muller limit, that Sanford was indeed correct that there is genetic deterioration in the human population. We can also then estimate hypothetically whether even an vigorous program of eugenics would cure the problem. If it won’t, then that suggests the human genome has been deteriorating for as far back as humans have been on Earth, and that means we didn’t evolve from some other species.

    If ENCODE is right that much of the genome serves functional roles, then as Dan Graur correctly (but unwittingly asserted): “If ENCODE is right, evolution is wrong.”

    Graur and others will keep claiming the C-value paradox, but that argument could be failing since we’re seeing evidence every species and even cell type within a species may utilize their genomes in different ways. For example, LINE-1 seems to induce genomic changes in every neuron in the human brain. Plants, as far as I know, don’t do such things to their genes, and certainly not in their brain cells since they have none.

    I mentioned LINE-1 role in brain development last year, and Allan Miller said he’d eat the hats of UDers without salt if I was proven right:

    Repetitive DNA and ENCODE

    If the L1 transposons active in neurons are anything remotely close to the 17% of the germline genome that consists of L1 LINEs, I will eat the hat of everyone at UD, without salt. How many transposons are we talking about?

    Well well well, Allan might think of how to roast Barry Arrington’s hat for a meal (yuck). Allan’s comment was in response to me bringing the LINE-1 issue up from an obscure 2012 paper, but it’s now becoming big news (h/t JoeCoder):

    The brain’s stunning genomic diversity revealed

    LA JOLLA—Our brains contain a surprising diversity of DNA. Even though we are taught that every cell in our body has the same DNA, in fact most cells in the brain have changes to their DNA that make each neuron a little different.

    Now researchers at the Salk Institute and their collaborators have shown that one source of this variation—called long interspersed nuclear elements or L1s—are present in 44 to 63 percent of healthy neurons and can not only insert DNA but also remove it. Previously, these L1s were known to be small bits of DNA called “jumping genes” that copy and paste themselves throughout the genome, but the researchers found that they also cause large deletions of entire genes. What’s more, such variations can influence the expression of genes that are crucial for the developing brain.

    The findings, published September 12, 2016 in the journal Nature Neuroscience, may help explain what makes us each unique—why even identical twins can be so different from one other, for example—and how jumping genes can go awry and cause disease.

    “In 2013, we discovered that different neurons within the same brain have various complements of DNA, suggesting that they function slightly differently from each other even within the same person,” says the study’s senior investigator Rusty Gage, a professor in Salk’s Laboratory of Genetics and holder of the Vi and John Adler Chair for Research on Age-Related Neurodegenerative Diseases. “This recent study reveals a new and surprising form of variation that will help us understand the role of L1s, not only in healthy brains but in those affected by schizophrenia and autism.”

  40. Hey Rumraket!

    redundant failsafe stuff has zero evidence that it correlates with genome size. And with respect to bacteria, it is generally understood that they have pretty much zero junk DNA.

    We know redundancy exists and I gave you evidence for this earlier. How could redundancy NOT increase genome size? I don’t follow your reasoning.

    Also, I said “microbes with huge genomes”, not necessarily bacteria. On amoebae for example:

    “amoebae are often cited as the most dramatic example of the lack of correlation between genome size and biological complexity. There are may problems with this conclusion, including a likely variation in ploidy, since some amoeba have hundreds of chromosomes, which may be generally related to cell size, not just in protists but in many different organisms, as well as the presence of significant amounts of contaminating DNA from their prey. The amoeba genome is probably smaller than 20 pg”

    20pg is about 20 billion base pairs. I doubt all of that is functional. But them also having a high number of ploidy is redundancy by definition.

    Would that not equally affect both deleterious and beneficial mutations?

    It would, but doubling the effective selection coefficient makes selection stronger for both beneficial mutations and deleterious mutations. It’s better at promoting beneficials and removing deleterious mutations. Or it’s possible I’ve made an error myself here. stcordova said previously that Mendel was shown to follow the expectations of Kimura’s formulas.

    JoeCoder seems to suggest the reason real populations don’t melt down is because god is intervening.

    I think there is no evidence that God is intervening (at present) to prevent populations from melting down. If you disagree, find me a microbe that persists in nature and has a deleterious (not total) mutation rate close to that of humans.

    Which would be funny if it wasn’t so ridiculous.

    I apologize that I don’t have a way for both atheism and evolution be true. Let me know if you figure something out though. 😛

    If it predicts meltdown for a 20% functional human genome, how much would have to be junk for no meltdown to happen? 10%? 5%?

    On a previous page I showed you a simulation in Mendel with 0.5% being functional, and the fitness declined at first but by 3000 to 5000 generations it looked like it was starting to level out. If you want to run a simulation longer than that to see for sure, go for it and post some screenshots. Maybe slightly higher values could also work?

    Rumraket, the part I don’t understand is why you think Mendel is suspect for showing fitness decline when mutation rates are high? That this decline happens in response to a high del. rate has been widely predicted in population genetics for the past several decades. See my comment #26 on page 7 of the comments, for details.

  41. Hello Dr. Felsenstein,

    Thus they are not trying to see what evolutionary forces enable populations to survive.

    1. What do you think is the deleterious mutation rate in humans? Or in other large mammals?
    2. How much is too much to survive?
    3. What realistic evolutionary forces would allow populations to survive higher rates?

  42. JoeCoder: I apologize that I don’t have a way for both atheism and evolution be true.

    Not sure if anyone else here will agree with me, but I find the ‘Evolution as Proof for the Existence of God’ idea pretty amusing.

    If you can’t beat ’em join ’em, I guess.

    You may find it equally amusing that I’d take the opposite tack. If I actually could be brought to believe that evolution required anything like the Judeo-Chistian diety, I’d infer that evolution must be false. Is it because I ‘hate God’? No–I just think it’s a really silly idea whose continuation is mostly a function of fear.

    Different strokes.

  43. walto: JoeCoder: I apologize that I don’t have a way for both atheism and evolution be true.

    God of the gaps, mathy version.

  44. Hey Walto,

    I think we can agree on much more than you may think. I think it would be ridiculous to try to argue evolution is evidence of God. Rather I am saying that this data on mutational load makes it impossible for evolution to work without help. Unless someone can show me otherwise.

    If I actually could be brought to believe that evolution required anything like the Judeo-Chistian diety, I’d infer that evolution must be false.

    That’s where I stand myself. However some here have previously argued “what about evidence of common descent!”

    1. In this thread I’ve previously discussed why I don’t find evidence of common descent (specifically fossils) compelling.
    2. But I am also saying that if you still find common descent compelling, that’s not a deal breaker to accept what I’m saying.

  46. JoeCoder:
    . . .
    I am saying that this data on mutational load makes it impossible for evolution to work without help.
    . . . .

    That doesn’t follow from any evidence you’ve provided. Until you provide a clear, detailed description of what MA is actually modeling under the covers, all you’ve got is a black box with blinkenlights. Stop looking at the shiny bits and find the man behind the curtain.

  47. amoebae are often cited as the most dramatic example of the lack of correlation between genome size and biological complexity.

    There is the potentially false assumption that species use the genomes in the same way, and Robert Tjian (president Howard Hughes Medical and biochem professor at UC Berkeley) made a passing remark that not even cell types in the same species use the genome the same way.

    The remark is here about 28 minutes into the video:

    …if you break open the nucleus of a very simple organism like yeast or you break open the nucleus of a human cell, that machinery look remarkably similar to each other, and yet the gene networks are very very different…..

    …are we really right in thinking that the core [transcriptional] machinery is universal and invariant. And that turns out to be an oversimplification…

    And when we look very carefully in the last few years particularly at individual different distinct cell types — let’s say muscle versus fat or neuron or liver cell,
    we certainly see differences in the activators as we would expect….but they’re not only working combinatorially with each other, but they are combining in different combinations with the core [transcriptional] machinery which is itself variable.

    And that was a kind of a revelation that’s really become more clear just in the last few years….

    there turns out to be a much greater degree of diversity in the core [transcriptional] machinery, the parts we thought were invariant, than we ever imagined.

    Now once you realize that that’s the case, that opens up a whole nother level of generating diversity which we didn’t anticipate.

    And that of course really allows multicellular organisms to diversify in unbelievable ways.

    The C-value paradox may be an indication of how non-conserved some of the gene regulatory networks and core transcriptional machinery is. It doesn’t necessarily say large genomes at junk, they may use the DNA in different ways than other creatures.

    TJian extends the number of human cell types beyond the canonical 213 types to thousands.

  48. Hey Patrick,

    That a high load leads to unstoppable fitness decline has been calculated for decades before Mendel was ever written. I outlined this to you on page 7, comment 26, but all you did was talk about Mendel instead. Mendel just adds another line of confirming evidence.

    I’ve given you the documentation for Mendel. It’s detailed, but it I agree that it could be improved by still being more detailed. Regardless I don’t know of any model where Mendel contradicts well accepted formulas in population genetics, and other examples where it confirms them have been cited in this thread.

    I find this sufficient. If you don’t then so be it. But at this point I’m not sure what else there is for us to discuss?

  49. JoeCoder:
    . . .
    I’ve given you the documentation for Mendel.It’s detailed, but it I agree that it could be improved by still being more detailed.Regardless I don’t know of any model where Mendel contradicts well accepted formulas in population genetics, and other examples where it confirms them have been cited in this thread.

    I don’t see where the model implemented in MA is documented in sufficient detail to support any claims about it.

    I find this sufficient.If you don’t then so be it.But at this point I’m not sure what else there is for us to discuss?

    Until the model implemented by MA is clearly documented there is nothing to discuss with respect to it. It cannot currently be analyzed by biologists with the relevant expertise, nor can an alternative implementation be created to confirm that MA implements the model correctly. As it stands, it is useless.

  50. Patrick:

    That doesn’t follow from any evidence you’ve provided. Until you provide a clear, detailed description of what MA is actually modeling under the covers, all you’ve got is a black box with blinkenlights. Stop looking at the shiny bits and find the man behind the curtain.

    Sheesh Patrick, the mutational load problem was independent of Mendel’s Accountant. Mendel’s Accountant was created to model the mutation load problem, not the other way around.

    The documentation on the mutational load problem has origins in the writings of Nobel Prize winner Hermann Muller. You can’t get any better documentation than that, and the mutation load question can and has been studied outside of Mendel’s Accountant.

    Larry Moran, Dan Graur, Hermann Muller didn’t need Mendel’s Accountant to assert the mutational load problem. You got documentation on the question right here in Joe Felsenstein’s book, page 154:

    http://evolution.gs.washington.edu/pgbook/pgbook.pdf

    question of the reality of mutational load as a problem for the population is made more pressing when we consider what used to be called the “c paradox.” ….

    Clearly an organism with as much DNA as we have would be in severe trouble. ….
    WHY WE AREN’T ALL DEAD. There are several possible resolutions of the dilemma. If much of the DNA is simply “spacer” DNA whose sequence is irrelevant, then there will be a far smaller mutational load. But notice that the sequence must be truly irrelevant, not just of unknown function. If the “extra” DNA has regulatory or chromosome-pairing function requiring it to have a specific base sequence, then mutations in that sequence will still cause a mutational load, even if these loci are not producing polypeptide chains.
    Thus the mutational load argument seems to give weight to the notion that this DNA is nonspecific in sequence. That is now believed to be the case, and the mutational load must give pause to anyone who proposes to find important functions for most of the DNA in eukaryotic genomes, especially functions that constrain its sequence.

    Joe Felsenstein
    Theoretical Evolutionary Genetics
    pages 154-155

    There is plenty of documentation to model the mutational load problem. You don’t need Mendel’s Accountant to explore the question. I snipped out most of the text above, but the link is there for you to follow the documentation on the problem.

    You want to ignore the mutation load question, that’s up to you, but you can’t use the amount of documentation on Mendel’s Accountant as much of an excuse to ignore the substance of what JoeCoder is saying because the mutational load problem predated the construction of Mendel’s Accountant.

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