horizontal gene transfer Intelligent Design News

Human evolution: Well, this IS a new take on “genetically modified organisms” (GMOs)

Spread the love

From the Economist:

Alastair Crisp and Chiara Boschetti of Cambridge University, and their colleagues, have been investigating the matter. Their results, just published in Genome Biology, suggest human beings have at least 145 genes picked up from other species by their forebears. Admittedly, that is less than 1% of the 20,000 or so humans have in total. But it might surprise many people that they are even to a small degree part bacterium, part fungus and part alga.

Dr Crisp and Dr Boschetti came to this conclusion by looking at the ever-growing public databases of genetic information now available. They did not study humans alone. They looked at nine other primate species, and also 12 types of fruit fly and four nematode worms. Flies and worms are among geneticists’ favourite animals, so lots of data have been collected on them. The results from all three groups suggest natural transgenics is ubiquitous.

It’s called horizontal gene transfer, and we have been covering it for years.

After all, it is a form of evolution for which there is lots of evidence, unlike the Darwin-in-the-schools textbook rot.

It is nice to be able to talk about evolution when there is actually a subject other than the impostures of the Darwin lobby. We hope to do much more on this in the future.

See also: Human evolution as a narrative

Follow UD News at Twitter!

88 Replies to “Human evolution: Well, this IS a new take on “genetically modified organisms” (GMOs)

  1. 1
    Dr JDD says:

    So how do we know that these genes have undergone HGT? Are there any viable alternative hypotheses that could fit seeing genes in humans and other organisms that do not fit on a standard phylogenetic tree?

  2. 2
    smiddyone says:

    It’s called horizontal gene transfer, and we have been covering it for years.

    Which confirms common descent

  3. 3
    Joe says:

    How does HGT confirm common descent? Please be specific

  4. 4
    smiddyone says:

    suggest human beings have at least 145 genes picked up from other species by their forebears.
    Where else would they come from?

  5. 5
    Box says:

    Everything seems to confirm common descent these days.

  6. 6
    Joe says:

    suggest human beings have at least 145 genes picked up from other species by their forebears.

    OK so you are saying it supports limited common descent as in humans are descendants of other humans.

  7. 7
    Joe says:

    Box, it’s all Common Descent and unguided evolution. 🙄

  8. 8
    Mark Frank says:

    It’s called horizontal gene transfer, and we have been covering it for years.

    Not, I think, as long as the scientific community.

    After all, it is a form of evolution for which there is lots of evidence, unlike the Darwin-in-the-schools textbook rot.

    Darwin-in-the-schools account of how evolution happens comprises two elements – unguided variation and natural selection. The natural selection bit applies equally to genes acquired horizontally or vertically. There is far more evidence for vertical transfer of genes then for horizontal transfer (or you trying to say there is no evidence for meiosis and mitosis?). Growing evidence for some horizontal gene transfer at the multicellular level is interesting and introduces another form of unguided variation which I guess will eventually find its way into textbooks (maybe has already?)

    It is nice to be able to talk about evolution when there is actually a subject other than the impostures of the Darwin lobby. We hope to do much more on this in the future.

    Or you could simply read the literature. After all it has nothing much to do with ID.

  9. 9
    DNA_Jock says:

    Could we have a quick informal poll: who here actually finds the Crisp et al. paper credible? Have the authors really demonstrated such widespread HGT in primates?

  10. 10
    Mark Frank says:

    #9 DNA_Jock

    who here actually finds the Crisp et al. paper credible?

    13 pages of technical material is a bit much for me. I will wait for the scientific community to respond.

  11. 11
    Joe says:

    Mark Frank:

    Darwin-in-the-schools account of how evolution happens comprises two elements – unguided variation and natural selection.

    Both of which have proven to be impotent. Did you have a point?

    After all it has nothing much to do with ID.

    It has nothing to do with unguided evolution.

  12. 12
    Joe says:

    Have the authors really demonstrated such widespread HGT in primates?

    Why are you so surprised? Any contact has the possibility of transferring biological material.

  13. 13
    ppolish says:

    “Common Ancestor” term needs to be retired.

    “Common Predecessors”, plural, matches up with the evidence so much better.

    C’mon, ancestors can be dead but NOT extinct.

  14. 14
    tjguy says:

    Has anyone read Casey Luskin’s article about HGT here?

    http://www.evolutionnews.org/2.....94701.html

    It was very enlightening for me! It seems like it is another example of “Heads I win, tails you lose” type of argument.

    When the same genes exist in supposed predecessors, it is evidence of common descent and then when there are totally different genes, instead of evidence against common descent, it is said to be evidence of HGT and therefore evidence of common descent!

    It is just another example of how contradictory data is finagled to provide “evidence” for common descent. They find a way to tweak the paradigm to make it work, but like Dr JDD asked

    how do we know that these genes have undergone HGT? Are there any viable alternative hypotheses that could fit seeing genes in humans and other organisms that do not fit on a standard phylogenetic tree?

    Smiddyone gives the following non-answer:

    suggest human beings have at least 145 genes picked up from other species by their forebears. Where else would they come from?

    Well, thinking within the Materialist paradigm, I guess there is no other answer. Their options are limited. So sure, just jump on the bandwagon and claim it as evidence for HGT and therefore unguided unintelligent evolution.

    But is it really? Just sayin’ so doesn’t make it so in real science.

    Maybe the data doesn’t really support common descent as well as we have been told!

  15. 15
    Dr JDD says:

    Smiddyone, thank you for demonstrating the 1-dimensional nature of the typical materialist thinking.

    The a priori assumption is that if a gene is present in an organism but not in what is determined to be a recent predecessor of that organism but in something much more distant – then it must be HGT. Unless of course there are very specific insertion sequences that suggest transmission via phage or something else known (or thought) to be a vehicle for HGT and thus a way to verify that these were indeed inserted, you are working on the assumption it was HGT due to phylogenetic trees.

    This is perhaps an example of how things are not falsifiable in the evolutionary paradigm. If you ask the question, “what would falsify common descent” one piece of evidence would surely be finding genes in distantly related species that were not present in more recently related species. There may be other explanations eg. HGT but you cannot assume that unless you are determined that you are not even going to entertain that the tree of life may be wrong.

    So smiddyone seeing as you seem to know so much about HGT please can you tell me how the researchers here determined this was HGT specifically other than the assumption that it must be given these organisms sit so distant on the tree of life? I am actually genuinely interested to know.

  16. 16
    wd400 says:

    I guess it’s time for the customary question: Why do you think HGT is a problem for mainstream evolutionary biology?

    This quote is particularly wierd:

    After all, it is a form of evolution for which there is lots of evidence, unlike the Darwin-in-the-schools textbook rot.

    Even you accept this study on face value you end up with ~99.5% of protein coding genes in humans having only verticle inheritance for the 600 million years or so. Part of the overwhelming evidence for common descent which, indeed, is taught in schools.

    On the other hand, this single paper says it possiblethat ~0.5% of those protein coding genes came into our ancestors horizontally, before being passed on vertically. In fact, they don’t really do enough to rule out other scenarios that could explain their results, so it’s not clear if even that half a percent came from prokaryotes.

    So, we have overwhelming evidence that the overwhelming majority of the genome has been passed on vertically. And some evidence that tiny fraction moved into our genome horizontally. And you want to sneer at the people teaching the overwhelming evidence for the overwhelming majority?

  17. 17
    Dr JDD says:

    Tjguy – was typing my response I guess as you were too – seems as though we are on the same track of thinking. This was the point of my first post yet smiddyone failed to contemplate that which proves the point of the limited scope of addressing evidence for potential multiple hypotheses.

    We couldn’t possibly falsify the tree of life and UCD therefore it MUST be something else.

    THe very fact something is not falsifiable makes it religious faith, not science. The very thing theists are accused of.

    By the way, I am not opposed to this being HGT nor am I saying it is not. I would like to know though how we can be certain it is HGT other than fitting in the paradigm of UCD and the ToL currently accepted and I would also like people to do science properly and understand all theories are falsifiable and you should always consider alternative hypotheses that fit the data.

  18. 18
    wd400 says:

    This is perhaps an example of how things are not falsifiable in the evolutionary paradigm. If you ask the question, “what would falsify common descent” one piece of evidence would surely be finding genes in distantly related species that were not present in more recently related species. There may be other explanations eg. HGT but you cannot assume that unless you are determined that you are not even going to entertain that the tree of life may be wrong.

    “finding genes in distantly related species that were not present in more recently related species” requires only gene loss in some lineages (ineed, the limiting taxonomic sampling in this paper is one reason to be suspicious of these results).

    More generally, it’s not a case of not “entertaining that the tree of life may be wrong” (which I guess means there is no tree?). It’s the fact common descent is so well supported by so much evidence. The prior that tree of life is “right” is so large that you will require a lot more than 100 genes that might have taken another route through time to change it very much.

  19. 19
    Dr JDD says:

    wd400:

    So if a rabbit fossil was found in a strata that predated say the Cambrian era that apparently as touted sneeringly by many materialists is an example of something that would falsify UCD etc.

    That is, 1 fossil.

    So would the argument be “but 99.99%of fossils fit the evolutionary UCD so this 1 fossil isn’t a problem”??

    My question remains, how do we know it is HGT? Since when in science do we need a certain percentage of evidence to falsify a theory? One apple falling the wrong way from a tree could falsify the theory of gravity despite the billions falling the “right” way.

    And again, ID and rejecting UCD is perfectly in line with what is observed with homology between species that does not simply align to common descent but also common design with some limited common descent, for example. So if it is fine with the 99.5% of “vertically” transferred genes what’s the big deal?

  20. 20
    Dr JDD says:

    By the way wd400 I would agree with you that HGT does not pose any problems to evolutionary theory or UCD, in my personal opinion.

    The problem I have is assuming that something that doesn’t fit with expectations of the tree of life and UCD must be HGT. That to me is bad science, and like you say it may not even be HGT but could be gene loss or other similar mechanisms that explain this.

    My points are to highlight the mentality of people in this field. It is a feature of many aspects of published work.

  21. 21
    wd400 says:

    It would be 99.99% of fossils support UCD, so it’s very probable this this one fossil was not really laid down in the Cambrian. That’s just how probability works.

    If you could actually prove the fossil was Cambrian then there would be a big problem from UCD, but you’d need lots of evidene to do so.

    Since when in science do we need a certain percentage of evidence to falsify a theory?

    Are you serious? Does ID go so far as to to doubt probability now?

    One apple falling the wrong way from a tree could falsify the theory of gravity despite the billions falling the “right” way.

    What would the wrong way be?

    So if it is fine with the 99.5% of “vertically” transferred genes what’s the big deal?

    You’ll have to ask News, I guess.

  22. 22
    Piotr says:

    Any contact has the possibility of transferring biological material.

    Targeting the germline? (otherwise it will not become heritable). “Any contact” can’t be enough, or your genome would be contaminated with banana DNA from eating bananas. Microbial infections are the likeliest kind of contact that can lead to horizontal transfer. HGT is known to have happened in eukaryotes (including primates), so it must be possible, though infrequent. The question is how infrequent.

    It isn’t true that the article claims “human beings” have picked up 145 genes from other species. As far as I can see, according to the authors only one (1) of them has been picked up by the human lineage since the human/chimp split, and the majority are “ancient” in the sense that the transfer took place anywhere between the origin of Chordata (about 520 Mya) and the common ancestor or Primates (about 65 Mya). That’s about 100 transfers in more than 400 My — one such event per four million years, on an average.

  23. 23
    Mapou says:

    Mark Frank:

    After all it has nothing much to do with ID.

    Horizontal gene transfer has everything to do with intelligent design. HGT is analogous to what software engineers call multiple inheritance. It is a well-known design technique.

    HGT destroys the strictly nested hierarchy of Darwinists that one would expect from common descent. But wouldn’t you know it? HGT is now part and parcel of Darwinian evolution. Of course.

  24. 24
    Joe says:

    Targeting the germline?

    It is a POSSIBILITY, Piotr. Unlike unguided evolution which isn’t even feasible.

  25. 25
    Joe says:

    Cupcake, you must be lost, as usual-

    Microbial infections are the likeliest kind of contact that can lead to horizontal transfer. HGT is known to have happened in eukaryotes (including primates), so it must be possible, though infrequent.- Piotr 22

  26. 26
    Piotr says:

    #23 Aurelio Smith,

    I’d like to see a convincing suggestion of how a gene could transfer horizontally and get into the gamete that becomes egg or sperm for the next generation.

    What about intracellular “reproductive parasites” specialising in infecting ovaries and mature eggs to make sure they are passed to their host’s offspring? The parasite may undergo “domestication” until it becomes an endosymbiont useful for the host — for example producing some enzymes by way of paying the rent. Wolbachia is one such case, and it’s a notorious source of (phage-mediated) horizontally transferred stuff in many arthropods and nematodes (including the insertion of its nearly complete genome into the DNA of one Drosophila species).

    http://www.ncbi.nlm.nih.gov/pm.....MC3068000/
    [Edited to add: http://www.sciencemag.org/content/317/5845/1753 ]

    Looks quite convincing to me.

  27. 27
    Mapou says:

    What are the mechanisms of HGT? I mean, how likely is it for a gene to be transferred from one animal to another, make its way to sperm or egg and finally result in an offspring with the newly acquired gene?

    Inquiring minds and all that.

  28. 28
    Dr JDD says:

    Piotr, I am convinced that this is a plausible mechanism for potential transfer of genetic information and have read of it before. HOwever what I would be interested in knowing is, are there any known concensous insertion sequences typical of such an event, or ways to strongly support a gene was inserted by the phage rather than already present? Without assuming it must be inserted because it appears t of sequence with phylogeny? I.e. does the insertion by phage leave a measurable signature that isn’t usually present in the host? A type of promoter site or similar unique to the phage?

  29. 29
    Piotr says:

    #29 Mapou,

    From animal to animal? Extremely unlikely. When the receiver is an animal, the usual sources are prokaryotes, protists, sometimes fungi (DNA transfer from plant to plant is not unknown). One could imagine transfer mediated by an endoparasite which borrows a genome fragment from one of its hosts (like Plasmodium vivax, which has some material “stolen” from Homo sapiens) and passes it on to another. But are there any sure examples?

  30. 30
    Piotr says:

    #30 Dr JDD,

    Ha! A good question to ask a specialist, if a specialist ever strays into this neighbourhood. The Wolbachia phage, WO, usually leaves its fingerprints (characteristic prophage elements) in the host’s genome, but I have no idea if there are any general methods of detecting such insertions.

    http://www.ncbi.nlm.nih.gov/pm.....MC2862486/

  31. 31
    wd400 says:

    Even rotifers, apparently kings of the HGT game among animals, appear to only have acquired genes from single-celled organisms: http://journals.plos.org/plosg.....en.1003035

  32. 32
    Piotr says:

    #34 Aurelio Smith,

    If my cursory reading of Crisp et al. 2015 is correct, they have identified only three HGT events in the human line since the MRCA of all primates. In other words, it means one “successful” event per 20 million years (of course there may have been others that failed to reach fixation).

  33. 33
    Zachriel says:

    Aurelio Smith: I’d like to see a convincing suggestion of how a gene could transfer horizontally and get into the gamete that becomes egg or sperm for the next generation.

    Retroviruses are commonly observed, and if they infect a germ cell, they can enter the germ line.

  34. 34
    Mapou says:

    Mapou:

    I mean, how likely is it for a gene to be transferred from one animal to another, make its way to sperm or egg and finally result in an offspring with the newly acquired gene?

    Piotr:

    From animal to animal? Extremely unlikely.

    Then how do you explain the transfer of complex bat DNA sequences involved in echolocation to whales many millions of years after the sequences first appeared in the tree of life? Never mind, I know the answer. It’s the all magical and powerful convergent-evolution voodoo God of the genome. Right?

  35. 35
    Zachriel says:

    Aurelio Smith: I was not thinking of ERVs as a subset of HGT.

    The protozoan Trypanosoma cruzi, which causes Chagas disease, can infect human germ cells, and then the DNA is passed down through generations. Other organisms do the same. It’s consistent with the selfish gene paradigm.

  36. 36
    Piotr says:

    #37

    From the article:

    To determine whether the detected HGT is ancient (prior to the divergence of the studied taxon), or has occurred throughout the evolution of a particular taxon, we mapped the foreign ortholog groups (representing founding HGT events) for each taxon onto the corresponding phylogenetic trees. In Drosophila species, there is a broad correspondence between length of branch (time) and the number of HGT events along each branch, suggesting that HGT has occurred throughout Drosophila evolution and is likely to be ongoing (Figure 1).

    The distribution of transfer events is different in the primates, with most foreign groups mapping to the base of the tree (a common ancestor of primates), suggesting that the majority of HGT in primates is ancient. In these cases we are not inferring that the HGT event occurred in the most recent common ancestor of all primates, but that it occurred sometime between the common ancestor of Chordata and the common ancestor of the primates, that is, prior to the time period shown in Figure 1. For example, in the case of HAS1 (Figure 3), which is found in a wide variety of chordates, the HGT event likely occurred soon after the common ancestor of Chordata arose.

    I suppose it’s easier said than done (see the “Discussion” section for a list of problems), but it seems a reasonable approach if you can compare a large number of closely related taxa. (I’m not sure if 10 primate species counts as a large number; if not, there’s room for improving the accuracy of the method.)

  37. 37
    Zachriel says:

    Mapou: Then how do you explain the transfer of complex bat DNA sequences involved in echolocation to whales many millions of years after the sequences first appeared in the tree of life?

    That is not an example of horizontal gene transfer, but parallel evolution.

    Mapou: Never mind, I know the answer. It’s the all magical and powerful convergent-evolution voodoo God of the genome. Right?

    No. The prestin gene involved is conserved in mammals, so the common ancestor of the bat and whale shared much the same gene. Both evolved echolocation, which requires higher frequency sensitivity, so the prestin evolved along the same pathway. However, if you look at the synonymous substitutions, they reveal the conventional phylogeny.

  38. 38
    Piotr says:

    Then how do you explain the transfer of complex bat DNA sequences involved in echolocation to whales many millions of years after the sequences first appeared in the tree of life?

    Please show that those sequences (I suppose you mean SLC26A5, the gene encoding for prestin, the cochlear motor protein) are “foreign” in whales (e.g. have no orthologues in other mammals) and present the evidence for HGT. OK, you needn’t bother. The prestin gene occurs in all mammals (including humans), and the researchers who compared the bat and whale sequences were careful to rule out HGT and several other explanations, leaving molecular convergence as the only remaining possibility.

  39. 39
    Joe says:

    The prestin gene occurs in all mammals (including humans), and the researchers who compared the bat and whale sequences were careful to rule out HGT and several other explanations, leaving molecular convergence as the only remaining possibility.

    Common design is more likely.

  40. 40
    Mapou says:

    Piotr:

    The prestin gene occurs in all mammals (including humans), and the researchers who compared the bat and whale sequences were careful to rule out HGT and several other explanations, leaving molecular convergence as the only remaining possibility.

    So we have complex identical sequences in two species residing in distant branches of the tree of life. Convergence, eh? This is akin to superstition. It’s chicken feather voodoo science.

    Piotr quoting the article:

    The distribution of transfer events is different in the primates, with most foreign groups mapping to the base of the tree (a common ancestor of primates), suggesting that the majority of HGT in primates is ancient.

    How do they explain the minority? Whole genes transferred between animals and they’re only interested in the base of the tree where HGT between simple organisms is known to be common?

    Where is the Minority Report? 😀

  41. 41
    Cross says:

    Piotr @ 43

    “leaving molecular convergence as the only remaining possibility”

    Or a common designer.

    Cheers

  42. 42
    Quest says:

    The really new take on GMOs is the possible connection to autism… My brother feels very strong about it… He has one autistic and one asbergers kid… Who can blame him…? Some selectively blame evolution for it but my brother doesn’t buy it… The circle of people I have been around for few years now makes me not to question science, which I do all the time anyways… It’s my middle name…

  43. 43
    wd400 says:

    “So we have complex identical sequences in two species”

    In fact, we do not. They are not identical — they just share some changes.

  44. 44
    Cross says:

    wd400 @ 48

    That’s what software designers do all the time, incorporate some code that works (class) and make modifications to suit.

    Cheers

  45. 45
    fifthmonarchyman says:

    Zac said,

    That is not an example of horizontal gene transfer, but parallel evolution.

    I say,

    Correct, just like the amazing parallel evolution of Neurons.

    check it out

    https://www.quantamagazine.org/20150325-did-neurons-evolve-twice/

    Apparently there are lots of things in nature that the average Joe would consider to be evidence against UCD but according to Darwinists are no problem at all.

    😉

  46. 46
    ppolish says:

    The Kingdom Plantae has quite a few Intelligently Designed species. Delicious and nutritious.

    Edit….my bad, I mean they’re all Intelligently Designed. But some are “made in the image” by Man.

  47. 47
    Zachriel says:

    Mapou: So we have complex identical sequences in two species residing in distant branches of the tree of life. Convergence, eh?

    They are not identical. The synonymous substitutions support the conventional phylogeny.

    Cross: Or a common designer.

    That doesn’t explain the pattern of synonymous substitutions.

  48. 48
    Zachriel says:

    fifthmonarchyman: Correct, just like the amazing parallel evolution of Neurons.

    Not “just like”. The prestin gene has many similarities in bats and whales (parallel), while the neurons of comb jellies are distinct but have a similar function (convergence). Moroz et al. is still tentative though intriguing.

  49. 49
    bFast says:

    HGT is interesting. Our technological world experiences horizontal technology transfer all of the time. We see transistors, LEDs, titanium etc. showing up all over the place. This technological interchange is the greatest difference we see between the way nature has assembled life, and the way humanity has assembled technology.

    HGT in the micro-organism world didn’t seem that compelling to me, but extensive HGT in advanced organisms? Quite unexpected. What would really be interesting, however, is if the HGT that has occurred was biologically significant. Its one thing to pick up something from somewhere else, but if what is picked up is “important” that is another matter.

  50. 50
    Mapou says:

    Zachriel and wd400,

    How many synonymous substitutions are we talking about here? Are we talking about a few pinpoint letters in a sequence or entire sequences within the genes? And how do you explain that these substitutions are in the exact same locations in the prestin genes of both species? Let’s calculate the odds.

    I know, the great convolution, uh… I mean convergence, spirit in the dirt did it.

  51. 51
    DATCG says:

    Seems like more assumptions about common ancestors…

    But what does it mean to “document” HGT in a multicellular organism? For them, again, it simply means finding a gene that contradicts the phylogeny. They don’t actually demonstrate that the gene arose by HGT. They just find a gene that seems more similar to one in another very different type of organism (like bacteria, protists, or fungi) than to more closely related organisms. Then they assume it got there by HGT.

    Under their (macro)evolutionary mindset, such severe phylogenetic conflict is not taken as evidence that something is wrong with the hypothesis of common ancestry. Rather, it is taken as evidence of HGT

    A Big Problem for Common Descent

    Hardly an isolated opinion by ID scientist as other non-design scientist agree and are recognizing the fall of Darwin’s Tree of Life. Looks more like a Forest of Life, multiple trees, not one…

    Darwin’s Tree of Life Wrong

    As others pointed out above with good questions and observations – research contradicting Darwinist faithful never matter. They appeal to more assumptions, showing a blind, “unguided” faith. Far from being skeptical and scientific, this is beginning to look like a cult of Darwinism.

  52. 52
    Mapou says:

    fifthmonarchyman, thank you for that Quanta Magazine link. Amazing stuff but this kind of stuff is to be expected because the Darwinist theory is wrong. We’ll see many more stuff like this now that genome sequencing is getting to be really cheap.

  53. 53
    Piotr says:

    #55 Mapou,

    Mammalian prestin is well conserved: more than 90% of the 700+ amino acids are identical between, say, humans and rats. Toothed whales, during their separate evolution, have acquired about fifty AA substitutions (varying from lineage to lineage), and roughly half of them can also be found among echolocating bats. Additionally, there is a positive correlation between the number of substitutions in toothed whales and the frequency at which they echolocate. For the pygmy sperm whale it’s 120 kHz, and about a dozen AA substitutions convergent with those in some bats (corresponding to non-synonymous mutations in the prestin gene; non-synonymous are those that make a difference). This suggests that the trait under selection was high-frequency hearing. The substitutions tend to occur in some parts of the protein rather than others, but they don’t form a sequence.

  54. 54
    Joe says:

    Mammalian prestin is well out of the reach of unguided evolution. And synonymous mutations can make a difference.

  55. 55
    wd400 says:

    And how do you explain that these substitutions are in the exact same locations in the prestin genes of both species? Let’s calculate the odds.

    Please do, you may surprise yourself…

    If you want to see other sequences of prestin genes they are available here

  56. 56
    bornagain77 says:

    “Shared Evolutionary History or Shared Design?” – Ann Gauger – January 1, 2015
    Excerpt: The waiting time required to achieve four mutations is 10^15 years. That’s longer than the age of the universe. The real waiting time is likely to be much greater, since the two most likely candidate enzymes failed to be coopted by double mutations.
    http://www.evolutionnews.org/2.....92291.html

  57. 57
    Mapou says:

    Piotr:

    The substitutions tend to occur in some parts of the protein rather than others, but they don’t form a sequence.

    It does not matter. We can calculate the odds of two different genes having the exact same mutations, no?

    1. Count the number of letters in the gene.
    2. Count the number of identical mutations.
    3. Calculate the probability of those mutations occurring twice in different species.

    If the probability approaches the number of particles in the known universe, you got yourself a big problem of not being credible. If not, you can continue to cruise on the leaky plausibility boat, which is all that convergent evolution is. It’s certainly not falsifiable science. It’s just a religion (materialism) betting on a lame pony in the race.

  58. 58
    bornagain77 says:

    Evolutionists Celebrated This Prediction But When it Later Failed They Didn’t Care – Cornelius Hunter – April 2012
    Excerpt: Sometimes their use of this lateral or horizontal gene transfer mechanism is a real stretch. And in any case, their story calls for evolution to have created this incredible mechanism which then was so important for adaptation and the supposed subsequent evolution. In other words, evolution created evolution.,,, In some cases evolutionists have no idea, beyond pure speculation, about how it could have happened. As they admit in one paper: “An alternative and more plausible possibility is that the STC gene has been laterally transferred among phylogenetically diverged eukaryotes through an unknown mechanism.”
    http://darwins-god.blogspot.co.....-this.html

    An Enzyme’s Phylogeny Reveals a Striking Case of Convergent Evolution – Jonathan M. – February 11, 2013
    Excerpt: The authors attempt to account for the incongruity by positing that “the STC gene has been laterally transferred among phylogenetically diverged eukaryotes through an unknown mechanism.” They thus attribute the shared genes to horizontal gene transfer (with no offered mechanism), a proposition that has become a catch-all to explain away severe conflicts between evolutionary phylogenies.,,,
    “phylogenetic conflict is common, and frequently the norm rather than the exception”
    (Dávalos et al., 2012).
    Is it possible that the real reason for such striking and widespread phylogenetic discordance is that evolutionary biologists are looking at biology through the wrong lens? Could the reason that there is so much difficulty in correlating organisms to a tree be that no such tree exists?
    http://www.evolutionnews.org/2.....68911.html

  59. 59
    Mapou says:

    bornagain77 quoting Hunter:

    Is it possible that the real reason for such striking and widespread phylogenetic discordance is that evolutionary biologists are looking at biology through the wrong lens? Could the reason that there is so much difficulty in correlating organisms to a tree be that no such tree exists?

    I disagree with Cornelius Hunter on the existence of the tree. There is certainly a tree. If you grafted a small branch from an orange tree to a lime tree, would this mean the lime tree is no longer a tree? Of course not. Grafting does not destroy the hierarchy. Grafting is an intelligent design thing, a beautiful thing indeed.

  60. 60
    bornagain77 says:

    Mapou, I guess as long as you are drawing ‘trees’ from imagination and not from any discernible real time empirical evidence that would warrant ‘real’ relationships, you can make the trees as ‘beautiful’ as you want, and then argue with other ‘artists’ as to whose trees are more ‘beautiful’. Just don’t call your ‘tree drawings’ science!

    Fudging Evolution to Avoid Falsification – March 12, 2015
    Evolutionary theory follows Finagle’s Rule #4: “Draw your curves, then plot your data.”
    Excerpt: “The fact that the clock is so uncertain is very problematic for us,” David Reich of Harvard said at a recent meeting where no consensus was reached. “It means that the dates we get out of genetics are really quite embarrassingly bad and uncertain.” The solution for some has been to invoke “rate heterogeneity”: mutations rates that speed up or slow down as needed to keep the theory intact. –
    http://crev.info/2015/03/fudging-evolution/

    Contradictory Trees: Evolution Goes 0 For 1,070 – Whif
    Excerpt: One of evolution’s trade secrets is its prefiltering of data to make it look good, but now evolutionists are resorting to postfiltering of the data as well.,,,
    Prefiltering is often thought of merely as cleaning up the data. But prefiltering is more than that, for built-in to the prefiltering steps is the theory of evolution. Prefiltering massages the data to favor the theory. The data are, as philosophers explain, theory-laden.
    But even prefiltering cannot always help the theory.,,,
    http://darwins-god.blogspot.co.....oes-0.html

    A New Model for Evolution: A Rhizome – Didier Raoult – May 2010
    Excerpt: Thus we cannot currently identify a single common ancestor for the gene repertoire of any organism.,,, Overall, it is now thought that there are no two genes that have a similar history along the phylogenic tree.,,,Therefore the representation of the evolutionary pathway as a tree leading to a single common ancestor on the basis of the analysis of one or more genes provides an incorrect representation of the stability and hierarchy of evolution. Finally, genome analyses have revealed that a very high proportion of genes are likely to be newly created,,, and that some genes are only found in one organism (named ORFans). These genes do not belong to any phylogenic tree and represent new genetic creations.
    http://darwins-god.blogspot.co.....izome.html

    Problem 6: Molecular Biology has Failed to Yield a Grand “Tree of Life” – Casey Luskin – February 2, 2015
    Excerpt: When fossils failed to demonstrate that animals evolved from a common ancestor, evolutionary scientists turned to another type of evidence — DNA sequence data — to demonstrate a tree of life. ,,,
    At the end of the day, the dream that DNA sequence data would fit into a nice-neat tree of life has failed, and with it a key prediction of neo-Darwinian theory.
    http://www.evolutionnews.org/2.....91151.html

    etc.. etc..

  61. 61
    DATCG says:

    Omaha, Omaha, Omaha = Convergent Evolution…

    “Convergence” story telling does not remove or solve problems for common ancestry by claims of HGT. It only calls an audible to shift Team Darwin’s blind formation to another assumed blind formation – Convergence – after intelligently reading opposing views.

    Penalty! Double Blind Shift! More than one Assumption in Motion. 100 million years back and loss of transitional fossils. This places you back to fictional story-telling.

    The problem for evolutionary biologists faced with conflicting evolutionary trees is that biological similarity often appears in places not predicted by common descent. In other words, everyone recognizes that biological similarities often appear among species in cases where they cannot be explained as the result of inheritance from a common ancestor. This means the main assumption fails.

    Problem 7 – Convergent Evolution

    The above link briefly highlights the story of bat/whale convergence. A story not a fact…

    Another famous example of convergent evolution is the ability of bats and whales to use echolocation, even though their distant common ancestor(unobserved assumption) did not have this trait. Evolutionary biologists long-believed this was a case of morphological convergence, but an article in Current Biology explains the “surprising” finding that echolocation in bats and whales also involves genetic convergence:

    “Only microbats and toothed whales have acquired sophisticated echolocation, indispensable for their orientation and foraging. Although the bat and whale biosonars originated independently and differ substantially in many aspects, we here report the surprising finding that the bottlenose dolphin, a toothed whale, is clustered with microbats in the gene tree constructed using protein sequences encoded by the hearing gene Prestin.”

    A common “hearing gene” used for hearing is not a “surprise” for Design.

    Forget again transitions do not exist or lack of common ancestor, except for fictional accounts. It makes a good story, because it must…

    Biochemist and Darwin-skeptic Fazale Rana reviewed the technical literature and documented over 100 reported cases of convergent genetic evolution.

    Each case shows an example where biological similarity — even at the genetic level — is not the result of inheritance from a common ancestor. So what does this do to the main assumption of tree-building that biological similarity implies inheritance from a common ancestor? With so many exceptions to the rule, one has to wonder if the rule itself holds merit.

    Indeed… what rule? which assumption? which story? told by materialist faith “holds merit?” HGT and Convergence make more exceptions to the rule, not less.

    These known problems lead to…

    Proponents of neo-Darwinian evolution are forced into reasoning that biological similarity implies common ancestry, except for when it doesn’t. And in the many cases where it doesn’t, they appeal to all sorts of ad hoc rationalizations to save common ancestry.

    But, there’s some logic creeping in, more evidence Darwin’s Tree of Life story is fading…

    There is some hope for a different story more attuned to the data, as Michael Syvanen dared to suggest in Annual Review of Genetics in 2012, that “life might indeed have multiple origins.” In other words, universal common ancestry may in fact, not be true.

    It is okay to be skeptical of Darwinian fairy tales, because more scientist, not only Intelligent Design scientist are questioning and rebelling against the Darwinist stories…

    “Darwinism and the neo-Darwinian synthesis, last dusted off 70 years ago, actually hinder discovery of the mechanism of evolution” (Antonio Lima-de-Faria, p. 83 – Geneticist, Altenburg 16).


    (emphasis mine)

  62. 62
    MrCollins says:

    I have question.

    So it’s taught that evolution happens over millions of year, but we have a little over 150ish years total studying it. So how can scientists really extrapolate over millions of years. Based on all the latest gene studies, it seems that either evolution would happen extremely fast or not at all and just be adaptation.

    I was just thinking and if we have 150 yrs of data and we’re talking about just 1 million yrs, then that’s only .015% of time collecting and studying data. Are we not grossly over estimating most of these ideas and theories? Just my random thoughts

  63. 63
    Piotr says:

    #62 Mapou,

    How about you doing the calculations? Consider the fact that the shared mutations did not all take place simultaneously (phylogenetic analysis shows it) and that they seem to be advantageous individually (various odontocete and bat lineages show only some of them). Therefore, their stepwise accumulation should be possible. You can assume any realistic population size and tempo of mutation.

  64. 64
    Mapou says:

    Piotr @68,

    The probability of the exact same genetic modification arising in disparate species does not depend on what order the mutations happened.

    It occurred to me earlier that the likelihood of convergent evolution arriving at any specific genetic modification more than once is astronomically low. And it does not matter how small or big the modification is, or whether it is in one gene or many genes.

    The genome can be seen as a base-4 number N. N is a humongous number because it is based on the number of base pairs in the genome, i.e., billions of base pairs. But any modification (i.e., one or more synonymous mutations) is also a number. The probability of selecting the same number more than once by chance is 1 in N, which is essentially no better than zero.

    You may wonder, why use the entire genome for the calculation? It is because random mutations operate on the entire genome, not just on the individual genes or the protein coding sequences or sections thereof. Again, it does not matter if the number of mutations comprising the modification is 1 or many. (Do you know why this is true, Piotr? LOL)

    But do correct me if I’m wrong. I’m always willing to change my mind in the face of contrary arguments.

  65. 65
    Mapou says:

    Again I ask, where is the Minority Report?

    See #45 above for an explanation.

  66. 66
    Piotr says:

    Mapou:

    It occurred to me earlier that the likelihood of convergent evolution arriving at any specific genetic modification more than once is astronomically low.

    No, it isn’t. For example, in the modern human population it takes about 20 years for a heritable mutation to happen somewhere, in someone, in each single nucleotide. At this rate, all possible point substitutions will have been tried in just a few hundred years. Beneficial mutations are more likely to spread and eventually dominate the population (selective pressure of course accelerates fixation). If a large percentage of the population already carries one beneficial innovation, it paves the way for any other mutation in the same gene which amplifies the advantage conferred by the first one. You don’t even have to wait until the first one outcompetes the ancestral allele. What matters is that both mutations will meet in some individuals, giving rise to a still better-adapted phenotype.

    I don’t know how many point mutations are actually shared by, say, the kogia (a.k.a. the pygmy sperm whale) and some particular bat lineage (as opposed to all echolocating bats taken together). Certainly not all — presumably three or four rather than twelve. Only two “bat-like” mutations were already present in the last common ancestor of all modern whales; others continued to crop up in the descendent lineages. Some of them, e.g. the beaked whales (echolocating at 20-40 kHz), show little or no further convergence with bats. The sperm whale (12.5 kHz) is a very close relative of the kogia, but has fewer AA innovations in its prestin and fewer convergent ones as well. Kogias and sperm whales split just a few million years ago, so the continued optimisation of ultrasonic hearing in kogias (120 kHz and more) is a recent, lineage-specific development. On the other hand, prestin evolved quickly in a “batty” direction in the common ancestor of the dolphins, but some kind of adaptive optimum was reached soon and there has been no further change in the last 15-20 million years.

    Note that prestin is strongly conserved in mammals (90+% AA sequence identity between distantly related lineages), which means that it already serves its function very well in typical mammalian ears, and the vast majority of possible modifications tend to be suppressed by negative selection. In echolocating species, however, there is some extra pressure favouring a specific kind of improvement (not important enough for other mammals to be visible to selection). If there was a strong selective pressure in some evolutionary lines favouring any improvement in high-frequency echolocation, but only a few AA changes could possibly have the desired effect, their convergent occurrence is hardly surprising. And it isn’t something that could not have happened by chance in a few million years.

  67. 67
    Piotr says:

    #70

    The explanation is probably the same as for other such transfers (intracellular parasites — protists or bacteria — infecting the germline). The details are hard to recover after millions of years, since we have only modern microbes for comparison. Our monkey ancestors may have harboured somewhat different bugs in their ovaries and testes.

  68. 68
    bornagain77 says:

    P claims:

    “Beneficial mutations are more likely to spread and eventually dominate the population (selective pressure of course accelerates fixation).”

    and yet that is not what we find:

    Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) – October 2010
    Excerpt: “Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, “This research really upends the dominant paradigm about how species evolve,” said ecology and evolutionary biology professor Anthony Long, the primary investigator.
    http://www.arn.org/blogs/index.....ruit_flies

    “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain – Michael Behe – December 2010
    Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain.
    http://behe.uncommondescent.co.....evolution/

    Study demonstrates evolutionary ‘fitness’ not the most important determinant of success – February 7, 2014 – with illustration
    Excerpt: An illustration of the possible mutations available to an RNA molecule. The blue lines represent mutations that will not change its function (phenotype), the grey are mutations to an alternative phenotype with slightly higher fitness and the red are the ‘fittest’ mutations. As there are so few possible mutations resulting in the fittest phenotype in red, the odds of this mutation are a mere 0.15%. The odds for the slightly fitter mutation in grey are 6.7% and so this is far more likely to fix, and thus to be found and survive, even though it is much less fit than the red phenotype.,,,
    By modelling populations over long timescales, the study showed that the ‘fitness’ of their traits was not the most important determinant of success. Instead, the most genetically available mutations dominated the changes in traits. The researchers found that the ‘fittest’ simply did not have time to be found, or to fix in the population over evolutionary timescales.
    http://phys.org/news/2014-02-e.....ccess.html

    This following headline sums the preceding finding up very nicely:

    Fittest Can’t Survive If They Never Arrive – February 7, 2014
    http://crev.info/2014/02/fitte.....er-arrive/

    Biological Information – Mutation Count & Synergistic Epistasis (Mutation accumulation) 1-17-2015 by Paul Giem – video
    https://www.youtube.com/watch?v=6gdoZk_NbmU

    Using Computer Simulation to Understand Mutation Accumulation Dynamics and Genetic Load:
    Excerpt: We apply a biologically realistic forward-time population genetics program to study human mutation accumulation under a wide-range of circumstances.,, Our numerical simulations consistently show that deleterious mutations accumulate linearly across a large portion of the relevant parameter space.
    http://bioinformatics.cau.edu......aproof.pdf

    Mutations : when benefits level off – June 2011 – (Lenski’s e-coli after 50,000 generations)
    Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually.
    http://www2.cnrs.fr/en/1867.htm?theme1=7

    New Research on Epistatic Interactions Shows “Overwhelmingly Negative” Fitness Costs and Limits to Evolution – Casey Luskin June 8, 2011
    Excerpt: In essence, these studies found that there is a fitness cost to becoming more fit. As mutations increase, bacteria faced barriers to the amount they could continue to evolve. If this kind of evidence doesn’t run counter to claims that neo-Darwinian evolution can evolve fundamentally new types of organisms and produce the astonishing diversity we observe in life, what does?
    http://www.evolutionnews.org/2.....47151.html

  69. 69
    Piotr says:

    BA77,

    I shouldn’t have said “of course” because there are various caveats complicating the discussion of selection and its effects (e.g. if selection coefficients are relatively low or vary over time). But as I write above, fixation doesn’t have to happen quickly, and one beneficial mutation does not have to wait till anothe one gets fixed.

  70. 70
    bornagain77 says:

    “because there are various caveats”

    That is a laugh, the entire theory of neo-Darwinism is one caveat built on another caveat,, one ‘caveat’ being ‘of course’ that the vast majority of supposed beneficial mutation are actually found to degrade the genome to a greater or lesser extent. And will thus be far more likely to degrade a genome than ever building up novel functional complexity/information (of which, another ‘caveat’, you have no real time examples of it ever happening)

    That IS NOT a minor caveat. Nor are Negative Epistatic Interactions of supposed beneficial mutations a minor caveat. Such Negative Epistatic Interactions clearly indicate that the staggering overlapping ‘polyfunctionality’ of the genome puts severe constraints on the evolvability of a organism to novel forms:

    Beneficial mutations that aren’t? -June 2011
    Three recent papers in Science: In Evolution, the Sum Is Less than Its Parts; Diminishing Returns Epistasis Among Beneficial Mutations Decelerates Adaptation; Negative Epistasis Between Beneficial Mutations in an Evolving Bacterial Population
    http://www.uncommondescent.com.....E2%80%99t/

    The diminishing returns of beneficial mutations – July 2011
    Excerpt: Evolution thus has three strikes against it: most mutations are not beneficial, practically all mutations destroy specified complexity, and, now, even ‘beneficial’ mutations work against each other. While mutations may be of limited benefit to a single organism in a limited context (e.g., sickle cell anemia can protect against malaria even though the sickle cell trait is harmful), mutations seem to be no benefit whatsoever for microbes-to-man evolution, whether individually or together.
    http://creation.com/antagonistic-epistasis

    Multiple Overlapping Genetic Codes Profoundly Reduce the Probability of Beneficial Mutation George Montañez 1, Robert J. Marks II 2, Jorge Fernandez 3 and John C. Sanford 4 – May 2013
    http://www.worldscientific.com.....08728_0006

    another minor ‘caveat’ for Darwinism is that it does not reflect reality:

    Lynn Margulis Criticizes Neo-Darwinism in Discover Magazine (Updated) – Casey Luskin April 12, 2011
    Excerpt: Population geneticist Richard Lewontin gave a talk here at UMass Amherst about six years ago, and he mathemetized all of it–changes in the population, random mutation, sexual selection, cost and benefit. At the end of his talk he said, “You know, we’ve tried to test these ideas in the field and the lab, and there are really no measurements that match the quantities I’ve told you about.” This just appalled me. So I said, “Richard Lewontin, you are a great lecturer to have the courage to say it’s gotten you nowhere. But then why do you continue to do this work?” And he looked around and said, “It’s the only thing I know how to do, and if I don’t do it I won’t get grant money.” –
    Lynn Margulis – biologist
    http://www.evolutionnews.org/2.....45691.html

    Coordinated mutations explode ‘waiting times’ for fixation into gargantuan proportions:

    Evolution And Probabilities: A Response to Jason Rosenhouse – August 2011
    Excerpt: The equations of population genetics predict that – assuming an effective population size of 100,000 individuals per generation, and a generation turnover time of 5 years – according to Richard Sternberg’s calculations and based on equations of population genetics applied in the Durrett and Schmidt paper, that one may reasonably expect two specific co-ordinated mutations to achieve fixation in the timeframe of around 43.3 million years. When one considers the magnitude of the engineering fete, such a scenario is found to be devoid of credibility.
    http://www.uncommondescent.com.....osenhouse/

    10^15 years for waiting time of four coordinated mutations (Axe Gauger)

    a few more minor ‘caveats’ for Darwinism in regards to population genetics:

    “it would in the end be far easier and more sensible to manufacture a complete man de novo, out of appropriately chosen raw materials, than to try to fashion into human form those pitiful relics which remained…
    it is evident that the natural rate of mutation of man is so high, and his natural rate of reproduction so low, that not a great deal of margin is left for selection…
    it becomes perfectly evident that the present number of children per couple cannot be great enough to allow selection to keep pace with a mutation rate of 0.1..if, to make matters worse, u should be anything like as high as 0.5…, our present reproductive practices would be utterly out of line with human requirements.”
    Hermann Muller quoted by John Sanford; Appendix 1, Genetic Entropy

    No Matter What Type Of Selection, Mutations Deteriorate Genetic Information – article and animation
    Excerpt: The animation asserts that if harmful mutation rates are high enough, then there exists no form or mechanism of selection which can arrest genetic deterioration. Even if the harmful mutations do not reach population fixation, they can still damage the collective genome.,,,
    Nobel Prize winner HJ Muller (of Muller’s ratchet fame) suggested that the human race can’t even cope with a harmful rate of 0.1 (mutations) per new born. The actual rate has been speculated to be on the order of 100-300.
    The animation uses a conservative harmful rate of 1 and argues (with some attempts at humor) that deterioration would thus be inevitable even with a harmful rate of 1 per new born.
    http://www.uncommondescent.com.....ns-weasel/

    Human evolution or extinction – discussion on acceptable mutation rate per generation (with clips from Dr. John Sanford) – video
    http://www.youtube.com/watch?v=aC_NyFZG7pM

  71. 71
    Joe says:

    Piotr:

    Our monkey ancestors may have harboured somewhat different bugs in their ovaries and testes.

    We are sure that YOU had monkey ancestors, but you only speak for yourself.

    Why do humans want to be related to monkeys and chimps? What twisted logic makes people do such a thing?

  72. 72
    bornagain77 says:

    Comprehensive Analysis of Chimpanzee and Human Chromosomes Reveals Average DNA Similarity of 70% – by Jeffrey P. Tomkins – February 20, 2013
    Excerpt: For the chimp autosomes, the amount of optimally aligned DNA sequence provided similarities between 66 and 76%, depending on the chromosome. In general, the smaller and more gene-dense the chromosomes, the higher the DNA similarity—although there were several notable exceptions defying this trend. Only 69% of the chimpanzee X chromosome was similar to human and only 43% of the Y chromosome. Genome-wide, only 70% of the chimpanzee DNA was similar to human under the most optimal sequence-slice conditions. While, chimpanzees and humans share many localized protein-coding regions of high similarity, the overall extreme discontinuity between the two genomes defies evolutionary timescales and dogmatic presuppositions about a common ancestor.
    http://www.answersingenesis.or.....chromosome

    More from Ann Gauger on why humans didn’t happen the way Darwin said – July 2012
    Excerpt: Each of these new features probably required multiple mutations. Getting a feature that requires six neutral mutations is the limit of what bacteria can produce. For primates (e.g., monkeys, apes and humans) the limit is much more severe. Because of much smaller effective population sizes (an estimated ten thousand for humans instead of a billion for bacteria) and longer generation times (fifteen to twenty years per generation for humans vs. a thousand generations per year for bacteria), it would take a very long time for even a single beneficial mutation to appear and become fixed in a human population.
    You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect.
    Facing Facts
    But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes— sixteen anatomical features—in the time available. At most, a new binding site might affect the regulation of one or two genes.
    http://www.uncommondescent.com.....rwin-said/

    Human Evolution: A Facebook Dialog – By Ann Gauger – Nov. 12, 2012
    Excerpt: PM:Is it also possible that the mechanism that you refer to in your video clip is not the only/main one at play?
    Biologic: The mechanism I refer to is based on the standard Darwinian model for evolution. Published population genetics estimates for how long it would take to make *and fix* a single base change to a DNA binding site in a 1 kb segment of DNA are prohibitively long—six million years. To get a second mutation in the same DNA binding site would take in excess of 200 million years.
    Now to go from hominid to human requires many changes, most of them to gene expression patterns. It is much easier to change the DNA binding site than to change the transcription factor’s specificity. And all these mutations must work together and be beneficial to the evolving organism. The window of time available according to the fossil record and phylogenetic estimates is too short for known mechanisms to be sufficient. So do I think there are are other things at play?
    Yes.
    http://www.biologicinstitute.o.....ialog?og=1

    Why Evolution Is Misunderstood – P.J. Levi – March 4, 2013
    Excerpt: Consider the evolution of humans and chimps from a common ancestor, to which Coyne in his talk referred several times. Rather than offering evidence for such common ancestry, Coyne simply took it as a fact and then used it to support Darwinian selection. Yet the ubiquity of selection in creating these species makes little sense at the level of DNA — the very level at which heritable change (evolution) occurs. By current estimates, the genomes of these two species differ by at least 300 million nucleotides. Given the premise that humans and chimps shared a common ancestor 6 million years ago, such a degree of divergence can only be accounted for by an average of 25 nucleotide changes per year in each line of descent.
    For Coyne’s gradual version of the Darwinian mechanism to account for these differences, 25 new mutations would have to appear, conferring a reproductive advantage, and spread through each population every year. Yet even 25 advantageous substitutions per generation is unfathomable.
    http://www.evolutionnews.org/2.....69771.html

    “Any transition of form is pure fantasy. There is no demonstration of it.”
    Douglas Axe – co-author of Science & Human Origins – video
    http://www.youtube.com/watch?v=XxMmLakH2LQ

    “Where (chimps and humans) really differ, and they differ by orders of magnitude, is in the genomic architecture outside the protein coding regions. They are vastly, vastly, different.,, The structural, the organization, the regulatory sequences, the hierarchy for how things are organized and used are vastly different between a chimpanzee and a human being in their genomes.”
    Raymond Bohlin (per Richard Sternberg) – 9:29 minute mark of video
    https://vimeo.com/106012299

    Richard Sternberg PhD – podcast – On Human Origins: Is Our Genome Full of Junk DNA? Part 2. (Major Differences in higher level chromosome spatial organization)
    5:30 minute mark quote: “Basically the dolphin genome is almost wholly identical to the human genome,, yet no one would argue that bottle-nose dolphins are our sister species”,,,
    http://www.discovery.org/multi.....-dna-pt-2/

    An Interview with Stephen C. Meyer
    TT: Is the idea of an original human couple (Adam and Eve) in conflict with science? Does DNA tell us anything about the existence of Adam and Eve?
    SM: Readers have probably heard that the 98 percent similarity of human DNA to chimp DNA establishes that humans and chimps had a common ancestor. Recent studies show that number dropping significantly. More important, it turns out that previous measures of human and chimp genetic similarity were based upon an analysis of only 2 to 3 percent of the genome, the small portion that codes for proteins. This limited comparison was justified based upon the assumption that the rest of the genome was non-functional “junk.” Since the publication of the results of something called the “Encode Project,” however, it has become clear that the noncoding regions of the genome perform many important functions and that, overall, the non-coding regions of the genome function much like an operating system in a computer by regulating the timing and expression of the information stored in the “data files” or coding regions of the genome. Significantly, it has become increasingly clear that the non-coding regions, the crucial operating systems in effect, of the chimp and human genomes are species specific. That is, they are strikingly different in the two species. Yet, if alleged genetic similarity suggests common ancestry, then, by the same logic, this new evidence of significant genetic disparity suggests independent separate origins. For this reason, I see nothing from a genetic point of view that challenges the idea that humans originated independently from primates,
    http://www.ligonier.org/learn/.....-conflict/

    The Red Ape – Cornelius Hunter – August 2009
    Excerpt: “There remains, however, a paradoxical problem lurking within the wealth of DNA data: our morphology and physiology have very little, if anything, uniquely in common with chimpanzees to corroborate a unique common ancestor. Most of the characters we do share with chimpanzees also occur in other primates, and in sexual biology and reproduction we could hardly be more different. It would be an understatement to think of this as an evolutionary puzzle.”
    http://darwins-god.blogspot.co.....d-ape.html

    “We have all seen the canonical parade of apes, each one becoming more human. We know that, as a depiction of evolution, this line-up is tosh (i.e. nonsense). Yet we cling to it. Ideas of what human evolution ought to have been like still colour our debates.”
    Henry Gee, editor of Nature (478, 6 October 2011, page 34, doi:10.1038/478034a),

    “A number of hominid crania are known from sites in eastern and southern Africa in the 400- to 200-thousand-year range, but none of them looks like a close antecedent of the anatomically distinctive Homo sapiens…Even allowing for the poor record we have of our close extinct kin, Homo sapiens appears as distinctive and unprecedented…there is certainly no evidence to support the notion that we gradually became who we inherently are over an extended period, in either the physical or the intellectual sense.”
    Dr. Ian Tattersall: – paleoanthropologist – emeritus curator of the American Museum of Natural History – (Masters of the Planet, 2012)

  73. 73
    Zachriel says:

    Mapou: How many synonymous substitutions are we talking about here? Are we talking about a few pinpoint letters in a sequence or entire sequences within the genes? And how do you explain that these substitutions are in the exact same locations in the prestin genes of both species?

    Do you mean non-synonymous substitutions? Synonymous substitutions fit the pattern expected of conventional phylogeny. Non-synonymous substitutions fit the pattern expected of natural selection.

    Mapou: We can calculate the odds of two different genes having the exact same mutations, no?

    1. Count the number of letters in the gene.
    2. Count the number of identical mutations.
    3. Calculate the probability of those mutations occurring twice in different species.

    If you are assuming the mutations are all independent, then that assumes a lack of a selective pathway.

  74. 74
    Piotr says:

    BA77,

    How shall I respond to that rigmarole, consisting of mined quotes, creationist misrepresentations of scientific research, weary old canards and Youtube University wisdom (most of ot only tangential to my discussion with Mung, at the very best)? It would probably be wiser to ignore you completely, but there’s one point I’d like to make.

    If you have a pair of alleles (alternative forms of the same locus) in a finite population, then — barring the special case of balancing selection — the elimination of one of them and the fixation of the other is a mathematical necessity. If selection is so weak that the evolution of the alleles is (quasi-)neutral, fixation will take more time but must eventually happen. There may be more than two alleles, e.g. if a new mutation happens at the same locus, but this doesn’t change the general scheme of things. Fixation or elimination happens sooner or later. It may take tens of thousands of generations in the wild (rather than a few hundred generations in a lab), but it will happen. In animals such as mammals, a polymorphism may survive for one or two million years before it is resolved, but not ten million years or more.

  75. 75
    bornagain77 says:

    as to “How shall I respond(?)”

    Actual empirical evidence instead of ad hominem would be nice for a change! 🙂

    as to:

    “the elimination of one of them and the fixation of the other is a mathematical necessity.”

    Retreating into theoretical mathematics instead of providing empirical evidence to counter the empirical evidence I cited?

    That dishonest tactic reminds me of this quote from Behe:

    Waiting Longer for Two Mutations – Michael J. Behe
    Excerpt: Citing malaria literature sources (White 2004) I had noted that the de novo appearance of chloroquine resistance in Plasmodium falciparum was an event of probability of 1 in 10^20. I then wrote that ‘for humans to achieve a mutation like this by chance, we would have to wait 100 million times 10 million years’ (1 quadrillion years)(Behe 2007) (because that is the extrapolated time that it would take to produce 10^20 humans). Durrett and Schmidt (2008, p. 1507) retort that my number ‘is 5 million times larger than the calculation we have just given’ using their model (which nonetheless “using their model” gives a prohibitively long waiting time of 216 million years). Their criticism compares apples to oranges. My figure of 10^20 is an empirical statistic from the literature; it is not, as their calculation is, a theoretical estimate from a population genetics model.,,,
    The difficulty with models such as Durrett and Schmidt’s is that their biological relevance is often uncertain, and unknown factors that are quite important to cellular evolution may be unintentionally left out of the model. That is why experimental or observational data on the evolution of microbes such as P. falciparum are invaluable,,,
    http://www.discovery.org/a/9461

    “The Edge of Evolution” Strikes Again 8-2-2014 by Paul Giem – video
    https://www.youtube.com/watch?v=HnO-xa3nBE4

    An Open Letter to Kenneth Miller and PZ Myers – Michael Behe July 21, 2014
    Dear Professors Miller and Myers,
    Talk is cheap. Let’s see your numbers.
    In your recent post on and earlier reviews of my book The Edge of Evolution you toss out a lot of words, but no calculations. You downplay FRS Nicholas White’s straightforward estimate that — considering the number of cells per malaria patient (a trillion), times the number of ill people over the years (billions), divided by the number of independent events (fewer than ten) — the development of chloroquine-resistance in malaria is an event of probability about 1 in 10^20 malaria-cell replications. Okay, if you don’t like that, what’s your estimate? Let’s see your numbers.,,,
    ,,, If you folks think that direct, parsimonious, rather obvious route to 1 in 10^20 isn’t reasonable, go ahead, calculate a different one, then tell us how much it matters, quantitatively. Posit whatever favorable or neutral mutations you want. Just make sure they’re consistent with the evidence in the literature (especially the rarity of resistance, the total number of cells available, and the demonstration by Summers et al. that a minimum of two specific mutations in PfCRT is needed for chloroquine transport). Tell us about the effects of other genes, or population structures, if you think they matter much, or let us know if you disagree for some reason with a reported literature result.
    Or, Ken, tell us how that ARMD phenotype you like to mention affects the math. Just make sure it all works out to around 1 in 10^20, or let us know why not.
    Everyone is looking forward to seeing your calculations. Please keep the rhetoric to a minimum.
    With all best wishes (especially to Professor Myers for a speedy recovery),
    Mike Behe
    http://www.evolutionnews.org/2.....88041.html

    Further note:

    Thou Shalt Not Put Evolutionary Theory to a Test – Douglas Axe – July 18, 2012
    Excerpt: “For example, McBride criticizes me for not mentioning genetic drift in my discussion of human origins, apparently without realizing that the result of Durrett and Schmidt rules drift out. Each and every specific genetic change needed to produce humans from apes would have to have conferred a significant selective advantage in order for humans to have appeared in the available time (i.e. the mutations cannot be ‘neutral’). Any aspect of the transition that requires two or more mutations to act in combination in order to increase fitness would take way too long (greater than 100 million years).
    My challenge to McBride, and everyone else who believes the evolutionary story of human origins, is not to provide the list of mutations that did the trick, but rather a list of mutations that can do it. Otherwise they’re in the position of insisting that something is a scientific fact without having the faintest idea how it even could be.” Doug Axe PhD.
    http://www.evolutionnews.org/2.....62351.html

  76. 76
    bornagain77 says:

    P., here is another small ‘caveat’ you forgot to mention. Even if you had empirical evidence that mutations to DNA could be fixed in a timely manner, you still have no empirical evidence that mutations to DNA can produce ‘body-plan morphogenesis’. In other words, your neo-Darwinian, (modern synthesis), assumption that mutations to DNA can produce new body-plans does not have any empirical support, but is just another unsupported assumption on your part!

    Response to John Wise – October 2010
    Excerpt: A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism.
    http://www.evolutionnews.org/2.....38811.html

    Stephen Meyer – Functional Proteins and Information for Body Plans – video
    https://vimeo.com/91322260

    Dr. Stephen Meyer comments at the end of the preceding video,,,
    ‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does not insure that proteins, cell types, tissues, organs, will all be arranged in the body. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’
    Stephen Meyer – (excerpt taken from Meyer/Sternberg vs. Shermer/Prothero debate – 2009)

    Body Plans Are Not Mapped-Out by the DNA – Jonathan Wells – video
    http://www.youtube.com/watch?v=meR8Hk5q_EM

    Ask an Embryologist: Genomic Mosaicism – Jonathan Wells – February 23, 2015
    Excerpt: humans have a “few thousand” different cell types. Here is my simple question: Does the DNA sequence in one cell type differ from the sequence in another cell type in the same person?,,,
    The simple answer is: We now know that there is considerable variation in DNA sequences among tissues, and even among cells in the same tissue. It’s called genomic mosaicism.
    In the early days of developmental genetics, some people thought that parts of the embryo became different from each other because they acquired different pieces of the DNA from the fertilized egg. That theory was abandoned,,,
    ,,,(then) “genomic equivalence” — the idea that all the cells of an organism (with a few exceptions, such as cells of the immune system) contain the same DNA — became the accepted view.
    I taught genomic equivalence for many years. A few years ago, however, everything changed. With the development of more sophisticated techniques and the sampling of more tissues and cells, it became clear that genetic mosaicism is common.
    I now know as an embryologist,,,Tissues and cells, as they differentiate, modify their DNA to suit their needs. It’s the organism controlling the DNA, not the DNA controlling the organism.
    http://www.evolutionnews.org/2.....93851.html

  77. 77
    leodp says:

    Thank you all for the great discussion. BA77, I’m in awe…how do you keep handy so many pertinant refs on so many different threads. Convergent quotes or horizontal meme transfer? Either way seems more ID than RM + NS.

  78. 78
    Silver Asiatic says:

    DATCG @ 56

    Thanks for pointing out that recent article by Casey Luskin on HGT

    Surprisingly, far from being a rare occurrence, it appears that HGT has contributed to the evolution of many, perhaps all, animals and that the process is ongoing, meaning that we may need to re-evaluate how we think about evolution.

    http://www.evolutionnews.org/2.....94701.html

    That statement: “we may need to re-evaluate how we think about evolution” is a good one. They can’t even make an unconditional statement. “We may or may not need to re-evaluate (a replay of our last evaluation), how we think (not what we think) about evolution.”

    In any case, Mr. Luskin writes some of the clearest explanations of how ‘we’ think about evolution that I’ve ever encountered. He gets a lot of ridicule from his opponents but I find him to be one of the very best educators on these otherwise, muddled and difficult topics.

    Whenever you hear “horizontal gene transfer” invoked in a context like this, what that really means is that biologists have uncovered genetic data sharply at variance with the standard evolutionary phylogenetic tree.

    Convergent evolution is another phrase that is used to perform the same kind of trick.

  79. 79
    Silver Asiatic says:

    Joe

    Why do humans want to be related to monkeys and chimps? What twisted logic makes people do such a thing.

    I’ve wondered that myself. I think people want to think that their origins are degraded – to the level of an animal. The classic (and evident) idea that humans have a unique and elevated origin and status can be difficult to live with. It puts demands on us to live up to a higher standard and to appreciate humanity as something special – not merely a modified-ape, different only in degree.

    Unguided evolution is basically an anti-human ideology. It reduces the highest and best desires and achievements of humanity to a desire to survive and reproduce. Nothing more than what bacteria are interested in.

    That's why it's evil – as I see it.

  80. 80
    Zachriel says:

    bornagain77: Even if you had empirical evidence that mutations to DNA could be fixed in a timely manner,

    We do, though fixation isn’t required, just prevalence within the population.

    bornagain77: you still have no empirical evidence that mutations to DNA can produce ‘body-plan morphogenesis’.

    Actually, we do. Small changes to prestin, for instance, change auditory characteristics.

  81. 81
    DNA_Jock says:

    Let’s accept, for the sake of argument, that the HGTs reported by Gos Micklem’s team are in fact evidence that life on earth has been subject to designed, intelligent intervention, whether by a deity or by advanced aliens.

    [That was certainly our reaction when we first learned about cross-kingdom HGT: our lab discussed what Erich “Chariots of the Gods?” von Däniken would make of these results… Gos may even have been present.]

    Evidently the earth has been visited a number of times – say between five and 100 times – in the past 400 million years or so by intervenor(s) with highly advanced germ-line genetic engineering capabilities. What can we infer about the capabilities and motivations of the these intervenor(s)?

    Two questions come to mind:

    Why, instead of inserting homeotic genes to create novel body plans, did the intervenor focus on such humdrum, run-of-the-mill metabolic processes?
    And why, oh why, the inordinate fondness for nematodes?

  82. 82
    DNA_Jock says:

    Not to mention the “We ain`t no stinking monkeys!” awkwardness.

    I`ll get me coat.

  83. 83
    Joe says:

    Let’s accept, for the sake of argument, that the HGTs reported by Gos Micklem’s team are in fact evidence that life on earth has been subject to designed, intelligent intervention, whether by a deity or by advanced aliens.

    Who is making that claim?

  84. 84
    DNA_Jock says:

    Casey Luskin is making that claim : “the case against common descent is compelling”…

  85. 85
    Joe says:

    Those are two DIFFERENT claims. What is wrong with you?

  86. 86
    Joe says:

    Actually, we do. Small changes to prestin, for instance, change auditory characteristics.

    That makes sense from an intelligent design perspective. Not sure how unguided evolution explains it though.

  87. 87
    Mapou says:

    Piotr @71:

    Mapou:

    It occurred to me earlier that the likelihood of convergent evolution arriving at any specific genetic modification more than once is astronomically low.

    No, it isn’t. For example, in the modern human population it takes about 20 years for a heritable mutation to happen somewhere, in someone, in each single nucleotide. At this rate, all possible point substitutions will have been tried in just a few hundred years.

    You people are so deluded, it’s beyond comprehension how you can call yourselves scientists. One substitution per person every 100 years does not a new species make. Nor will it turn fins into legs or legs into wings. Besides, the number of point substitutions in a genome is only equal to the number of base pairs. This is lame. To properly search the genome for new functions one must search through all possible combinations of point substitutions and this number is greater than the number of particles in the known universe. It gets much worse if you want to create entirely new genes. Live with it.

  88. 88
    Piotr says:

    You people are so deluded, it’s beyond comprehension how you can call yourselves scientists. One substitution per person every 100 years does not a new species make.

    You misunderstand. 100 years is just about enough time for every possible point mutation to occur somewhere in the human population. In every new human zygote there are about 130 new point mutations not present in the parents. And we haven’t yet begun to discuss other mutation types, the effects of recombination, retrovirus insertions, etc.

Leave a Reply