'Junk DNA' Genetics

Cost of maintenance and construction of design, neutral theory supports ID and/or creation

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Most of biological ID literature is focused on Irreducible Complexity and Specified Complexity (Specified Improbability) and information theory, no free lunch, critique of OOL, the Cambrian explosion, etc,

But there is another line of argument that is devastating to the claims of mindless evolution that has been underappreciated partly because it is highly technical, and in many cases most biologists will not even learn it in detail, namely that most molecular evolution is non-Darwinian.

Here is the simplest way to understand why evolution is mostly non-Darwinian. The ability to select for or against a trait involves the cost of sacrificing individual lives. When we spend money we have a limited budget to buy things. From our budget we can select to have maintenance done on our houses, cars, computers, our bodies (healthcare) or we can buy other thing to accumulate possessions.

What Darwin and most Darwinists do not realize is that selection for individual traits likewise comes at cost. To select to maintain one part of the genome means that there is no budget to maintain another part of the genome. To select to construct new features of the genome means one must abandon the maintenance budget of another part. This will be true even if the selection process is done by an intelligent agency like a human. The reason most computerized “proofs” of evolutionism like Dawkins Weasel and Avida are invalid is they do not model the problem of cost of maintaining and constructing mutli gigabit complex designs.

To understand things more clearly, here is a hypothetical illustration. If an asexually reproducing species could only have one offspring, selection must necessarily be neutral because there is no reproductive excess, there is zero “money” to carry out selection. If there are harmful mutations along the way, oh well, no “money” of excess reproduction to fix it. This would be an extreme case of Muller’s ratchet where the bad irreversibly just keeps accumulating.

Now if an asexually reproducing species could have two offspring, it now has a little more “money” in the form of reproductive excess to select to maintain one trait that goes bad. Let’s say one of the two offspring develops a bad mutation and the other doesn’t. We can expend him, or dare I say “spend” him to fix the genome. But our selection budget would be blown if each of the kids develop 1 bad mutation each, and it would really be blown if they develop 100 bad mutations each! And at this point we are not even considering the budget needed to build new functional traits.

When we actually do careful accounting of the costs of natural selection envisioned by Darwin and Dawkins versus the available money of reproductive excess, we realize that if evolution happens, it must be mostly free of selection as a matter of principle, and thus mostly neutral. There is simply not enough “money” in the form of reproductive excess to maintain and construct complex designs composed of billions of nucleotide and epigenetic “traits”. There is some selection obviously, because there is some “money” to do a little bit, but not enough.

The accounting of the cost of selection can be done in a number of ways. One way to demonstrate this is through the equations of population genetics, and the other way is a computer simulation that does the accounting. One of the best, if not the best computer accounting simulations is Mendel’s Accountant written by the dream team of creationist population genetics. The irony then is population geneticists, PZ Myers, Larry Moran, the YECs have had a rare moment of agreement where they have all signed the claim, “most molecular evolution is non-Darwinian.”

But if most evolution is non-Darwinian, maintenance much less construction of design cannot be explained by Darwinism, then the case for ID is strengthened.

Now if most evolution had been non-Darwinian, one would rightly argue it would have been a random walk, and thus not much better than a tornado going trough a junkyard. Creationist have seized on this and said, “well we’re not a junkyard, therefore some non-random process must have created designs in nature, hence we are designed”. In contrast, Larry Moran and friends have said “evolution is a random walk and we are obviously junkyards and you’re an IDiot if you think biological organisms are mostly functional.”

[cross posted at CEU IDCS Cost of maintenance and construction of design, neutral theory supports ID and/or creation]

75 Replies to “Cost of maintenance and construction of design, neutral theory supports ID and/or creation

  1. 1
    JoeCoder says:

    So much for “free peer review”. Larry Moran is complaining about this blog post but doesn’t offer a counter-argument. Nor has anyone yet done so in the comments.

    If I were to guess, maybe he takes issue with the “tornado in a junkyard” analogy since under neutral evolution the more deleterious mutations are still selected away? Or possibly it’s because he believes most of the genome is junk–a view that seems to be losing favor among evolutionary biologists. As Dr. Moran previously blogged:

    In my opinion, the evidence for massive amounts of junk DNA in our genome is overwhelming but I struggle to convince other scientists of this … I recently attended a meeting of evolutionary biologists and I’m pretty sure that the majority still don’t feel very comfortable with the idea that 90% of our genome is junk.

    I wonder what percentage of junk is closest to the consensus among ev biologists? 70%? 50%? 20%? Even under young earth creation you would expect some junk since the population genetics models show functional coding elements being destroyed much more quickly than they could be created.

    Now if you’ll excuse me I need to go to the kitchen to get some more popcorn.

  2. 2
    Acartia_bogart says:

    You lost your argument in the third sentence by demonstrating your complete lack of knowledge about natural selection.

    ” The ability to select for or against a trait involves the cost of sacrificing individual lives.”

    Even first year biology students know that natural selection is not dependent on the sacrifice of individual lives. It only requires an increased rate of reproduction as compared to those that lack the trait b

  3. 3
    NickMatzke_UD says:

    “Or possibly it’s because he believes most of the genome is junk–a view that seems to be losing favor among evolutionary biologists.”

    Actually, what’s actually happening is that the evolutionary biologists are winning over the ENCODE people, who are in full retreat on their “most of the genome is functional” position.

    http://judgestarling.tumblr.co.....te-our-lab

  4. 4
    NickMatzke_UD says:

    But, the fact that Sal couldn’t even bother to mention the possibility that most of the genome is junk, which is a direct implication of the position that most of the genome is evolving neutrally (as well as lots of other evidence), is yet another thing that will encourage Larry Moran to keep using the term “IDiot.”

  5. 5
    jerry says:

    the possibility that most of the genome is junk, which is a direct implication of the position that most of the genome is evolving neutrally

    Isn’t this a testable hypothesis. Shouldn’t one be able if he/she had the skills and access to the data be able to determine which sections are mutating and which are not?

    For example, if we took multiple genomes from humans or mice or rats (these are the three genomes for which there is the most data) that are from very different parts of the world one should be able to compare the non-coding regions to see which are conserved and which are mutating away.
    human
    There are genomes from Africa, Europe, Australia and New Guinea which represent 10’s of thousands of years of isolation. Then there is the Neanderthal genome.

    Is there a reason why we couldn’t use them to compare the different non-coding regions of the genome to see what has been conserved?

  6. 6
    bornagain77 says:

    Yes Nick the genome must surely be junk because the evidence free wishful speculation of non-falsifiable Darwinian speculations predict it. Then, on the other hand, for those not so enamored with the baseless fantasies of atheists, reality beckons!

    DNA – Replication, Wrapping & Mitosis – video
    https://vimeo.com/33882804

    DNA Packaging: Nucleosomes and Chromatin
    Excerpt: each of us has enough DNA to go from here to the Sun and back more than 300 times, or around Earth’s equator 2.5 million times! How is this possible?
    http://www.nature.com/scitable.....omatin-310

    Chromosome and Kinetochore
    https://www.youtube.com/watch?v=0JpOJ4F4984

    3-D Structure Of Human Genome: Fractal Globule Architecture Packs Two Meters Of DNA Into Each Cell – Oct. 2009
    Excerpt: the information density in the nucleus is trillions of times higher than on a computer chip — while avoiding the knots and tangles that might interfere with the cell’s ability to read its own genome. Moreover, the DNA can easily unfold and refold during gene activation, gene repression, and cell replication.
    http://www.sciencedaily.com/re.....142957.htm

  7. 7
    bornagain77 says:

    Information Storage in DNA by Wyss Institute – video
    https://vimeo.com/47615970

    Quote from preceding video:
    “The theoretical (information) density of DNA is you could store the total world information, which is 1.8 zetabytes, at least in 2011, in about 4 grams of DNA.”
    Sriram Kosuri PhD. – Wyss Institute

    Scientists’ 3-D View of Genes-at-Work Is Paradigm Shift in Genetics – Dec. 2009
    Excerpt: Highly coordinated chromosomal choreography leads genes and the sequences controlling them, which are often positioned huge distances apart on chromosomes, to these ‘hot spots’. Once close together within the same transcription factory, genes get switched on (a process called transcription) at an appropriate level at the right time in a specific cell type. This is the first demonstration that genes encoding proteins with related physiological role visit the same factory.
    http://www.sciencedaily.com/re.....160649.htm

    600 Genes Involved in Fundamental Cell Division – Cornelius Hunter – July 2011
    Excerpt: The hundreds of genes are involved in an absolutely fundamental biological process is yet another example of evolution’s failure to explain biology.
    http://darwins-god.blogspot.co.....-cell.html

    Centriole – video
    https://www.youtube.com/watch?v=NNvXTassmHM

    Multidimensional Genome – Dr. Robert Carter – video
    http://www.metacafe.com/watch/8905048/

    The Extreme Complexity Of Genes – Dr. Raymond G. Bohlin – video
    http://www.metacafe.com/watch/8593991/

    At the 10:30 minute mark of the following video, Dr. Trifonov states that the idea of the selfish gene ‘inflicted an immense damage to biological sciences’, for over 30 years:

    Second, third, fourth… genetic codes – One spectacular case of code crowding – Edward N. Trifonov – video
    https://vimeo.com/81930637

    In the preceding video, Trifonov elucidates codes that are, simultaneously, in the same sequence, coding for DNA curvature, Chromatin Code, Amphipathic helices, and NF kappaB. In fact, at the 58:00 minute mark he states, “Reading only one message, one gets three more, practically GRATIS!”. And please note that this was just an introductory lecture in which Trifinov just covered the very basics and left many of the other codes out of the lecture. Codes which code for completely different, yet still biologically important, functions. In fact, at the 7:55 mark of the video, there are 13 codes that are listed on a powerpoint, although the writing was too small for me to read.

  8. 8
    jerry says:

    the baseless fantasies of atheists

    I agree that a lot of the rhetoric used by those who believe in a naturalist approach to evolution is based on this. But, Nick Matzke claims he is not an atheist. So it is hard to use that particular argument here.

    Some of the non-coding regions are not functional and some are. The question is how much of each. That is what we should be focusing on.

  9. 9
    jerry says:

    Actually, what’s actually happening is that the evolutionary biologists are winning over the ENCODE people, who are in full retreat on their “most of the genome is functional” position.

    Here is another question for you. What percentage of novel coding regions arose from the process that produces these non-coding no function sequences. Is this the main source for coding regions or is there another source?

  10. 10
    bornagain77 says:

    “Nick Matzke claims he is not an atheist.”

    Nick Matzke also falsely claims, via the fraudulent practice of literature bluffing, that Darwinian processes created the Bacterial Flagellum:

    Calling Nick Matzke’s literature bluff on molecular machines – DonaldM UD blogger – April 2013
    Excerpt: So now, 10 years later in 2006 Matzke and Pallen come along with this review article. The interesting thing about this article is that, despite all the hand waving claims about all these dozens if not hundreds of peer reviewed research studies showing how evolution built a flagellum, Matzke and Pallen didn’t have a single such reference in their bibliography. Nor did they reference any such study in the article. Rather, the article went into great lengths to explain how a researcher might go about conducting a study to show how evolution could have produced the system. Well, if all those articles and studies were already there, why not just point them all out? In shorty, the entire article was a tacit admission that Behe had been right all along.
    Fast forward to now and Andre’s question directed to Matzke. We’re now some 17 years after Behe’s book came out where he made that famous claim. And, no surprise, there still is not a single peer reviewed research study that provides the Darwinian explanation for a bacterial flagellum (or any of the other irreducibly complex biological systems Behe mentioned in the book). We’re almost 7 years after the Matzke & Pallen article. So where are all these research studies? There’s been ample time for someone to do something in this regard.
    Matzke will not answer the question because there is no answer he can give…no peer reviewed research study he can reference, other than the usual literature bluffing he’s done in the past.
    http://www.uncommondescent.com.....ent-453291

    Thus since Nick has shown he could care less for the actual truth of a matter, why should his claim for anything be taken seriously?

  11. 11
    Joe says:

    Nick Matzke,

    Just how does blind and undirected processes account for any genome? Please present a testable model.

    Also Larry Moran is a proven imbecile so he isn’t in any position to insult anyone.

  12. 12
    jerry says:

    “Nick Matzke claims he is not an atheist.”

    That is not the issue here. What is the issue is how much of the human genome is non-functional. Let’s have a discussion on that. We have research which says a significant part of the non-coding regions is functional and are subject to positive selection. The question is how much more.

  13. 13
    Joe says:

    Natural selection does NOT select. It is eliminative, meaning whatever can’t cut it in the environment it is in will be eliminated from the population (unless it can move to an environment in which it can survive).

    Natural selection has proven to be impotent as a designer mimic. And that means that evolutionism is a failure as it has nothing left as an alleged designer mimic.

  14. 14
    jerry says:

    Please present a testable model.

    There are very testable hypothesis on this. And I am sure there will be lots of research on this in the next few years as various genomes get listed in the genome data bases. When it does, Axe will either be supported or he will be falsified. I expect he will be supported but the information is coming for this.

  15. 15
    bornagain77 says:

    Acartia_bogart @2, perhaps you would like to tell us how Natural Selection, a process selecting 3-Dimensional phenotypes, produces 4-Dimensional systems?:

    “Although living things occupy a three-dimensional space, their internal physiology and anatomy operate as if they were four-dimensional. Quarter-power scaling laws are perhaps as universal and as uniquely biological as the biochemical pathways of metabolism, the structure and function of the genetic code and the process of natural selection.,,, The conclusion here is inescapable, that the driving force for these invariant scaling laws cannot have been natural selection.” Jerry Fodor and Massimo Piatelli-Palmarini, What Darwin Got Wrong (London: Profile Books, 2010), p. 78-79

    The predominance of quarter-power (4-D) scaling in biology
    Excerpt: Many fundamental characteristics of organisms scale
    with body size as power laws of the form:

    Y = Yo M^b,

    where Y is some characteristic such as metabolic rate, stride length or life span, Yo is a normalization constant, M is body mass and b is the allometric scaling exponent.
    A longstanding puzzle in biology is why the exponent b is usually some simple multiple of 1/4 (4-Dimensional scaling) rather than a multiple of 1/3, as would be expected from Euclidean (3-Dimensional) scaling.
    http://www.nceas.ucsb.edu/~dre.....18_257.pdf

    The reason why 4-Dimensional things are completely invisible to 3-Dimensional things is best illustrated by ‘flatland’:

    Flatland – 3D to 4D shift – Carl Sagan – video
    http://www.youtube.com/watch?v=UnURElCzGc0

  16. 16
    jerry says:

    Natural selection has proven to be impotent as a designer mimic.

    I don’t think naturalist like Allen MacNeill say it is a designer. It is more like the explanatory filter which allows certain arguments to get through while rejecting other arguments. NS allows certain new variation to get through while rejecting others. It is not the source of variation.

    There is a similar problem with drift in the evolution debate in that it fixes already accepted variation and nothing else. The EF is not the source of arguments but the blessing of successful arguments. Neither the EF or NS create anything. So evolution is an after effect of the NS process which allowed some variation to survive while rejecting others.

    The whole debate is over the origin of new alleles, not how they survive or get fixed. We can now extend the allele argument to non-coding functional regions. How did they arrive?

  17. 17
    bornagain77 says:

    jerry, you never answered why I should take Nick’s claims for anything seriously since he has shown a willingness to lie in the past to protect a philosophical bias (which happens to be atheistic/materialistic). You may consider such dishonesty a trivial matter, but I do not.

  18. 18
    jerry says:

    Here are a couple posts by Allen MacNeill on the topic of NS and variation:

    http://www.uncommondescent.com.....ent-496789

    http://www.uncommondescent.com.....ent-306698

    Now MacNeill may vary from people like Nick Matzke but both are naturalist and we will have to see which of these view points NS lets survive. Maybe NS will eliminate both of them.

  19. 19
    scordova says:

    jerry, you never answered why I should take Nick’s claims for anything seriously since he has shown a willingness to lie in the past to protect a philosophical bias (which happens to be atheistic/materialistic). You may consider such dishonesty a trivial matter, but I do not.

    Nick’s personal beliefs as well as anyone else’s aren’t on topic unless they volunteer it in this discussion or it has relevance to the cost issue or function issue. Please drop it in this discussion.

    You can take issue with his scientific claims about junk.

    Sorry, Nick. Thanks for visiting.

  20. 20
    jerry says:

    You may consider such dishonesty a trivial matter, but I do not.

    I do not consider it a trivial matter when someone lies. I have children who have done it many times with me and I have found it best to be polite about it when they are caught. It gets you much further.

    But on this topic under discussion we have no evidence yet of such and accusing someone of lying gets you no where. I would like Nick to answer some basic questions which he should be able to. I hope he does.

  21. 21
    scordova says:

    the fact that Sal couldn’t even bother to mention the possibility that most of the genome is junk,

    Correction Nick, I pointed out the position of some of you guys:

    “evolution is a random walk and we are obviously junkyards and you’re an IDiot if you think biological organisms are mostly functional.”

  22. 22
    bornagain77 says:

    “accusing someone of lying gets you no where”

    It is not an accusation but a documented fact!

    Sorry Sal, but I DO NOT LIKE BEING LIED TO! Especially in matters relating to scientific evidence. I will bother your post no more.

  23. 23
    scordova says:

    Even first year biology students know that natural selection is not dependent on the sacrifice of individual lives. It only requires an increased rate of reproduction as compared to those that lack the trait b

    LOL! So individuals that lack a trait that reproduce at a lower rate in a limited population aren’t essentially sacrificed according to you. The ones with excess reproductive rates essentially scarifice those with less. That was clearly the sense I was using it. You either fail basic math or you show yourself misrpresenting what I said.

    I said:

    reproductive excess

    So is most molecular evolution non-Darwinian or not?

  24. 24
    Joe says:

    There are very testable hypothesis on this.

    Really? Where are the testable hypotheses for blind and undirected processes producing genomes? Are they locked up somewhere? They are definitely hidden from public view.

    I don’t think naturalist like Allen MacNeill say it is a designer.

    When Allen comes up with his theory I will listen. Until then NS is a proposed designer mimic.

    The whole debate is over the origin of new alleles, not how they survive or get fixed.

    No, the whole debate is about what is the cause of design in nature/ biology

  25. 25
    scordova says:

    BA77,

    These sorts of comments are welcome in the discussion.

    “Although living things occupy a three-dimensional space, their internal physiology and anatomy operate as if they were four-dimensional. Quarter-power scaling laws are perhaps as universal and as uniquely biological as the biochemical pathways of metabolism, the structure and function of the genetic code and the process of natural selection.,,, The conclusion here is inescapable, that the driving force for these invariant scaling laws cannot have been natural selection.” Jerry Fodor and Massimo Piatelli-Palmarini, What Darwin Got Wrong (London: Profile Books, 2010), p. 78-79

    Thank you for that.

  26. 26
    JoeCoder says:

    In my first post above (#1), the link to Dr. Moran’s blog should have been here. I didn’t realize it at first, but actually dates to before the ENCODE phase 2 announcement.

  27. 27
    jerry says:

    Really? Where are the testable hypotheses for blind and undirected processes producing genomes?

    They will be in the genomes of supposedly related species. Any new coding region must have remnants in related species that never reached the point where they could code. They are either there or not there. As genomes of various species get published it will be easy to verify this one way or the other.

    If there is nothing this will indicate that the coding region appeared out of nowhere. If it appeared naturally there will be corresponding non-coding regions in other species that do not code for anything.

    As I said with current technology and the way it is headed getting these genomes will be fast and inexpensive. They now code a significant section of the human genome for about $10-$15. That is what it cost 23andme and Ancestry dot com to process samples sent in to them. The amount should increase with time and the cost should go down.

  28. 28
    jerry says:

    When Allen comes up with his theory I will listen. Until then NS is a proposed designer mimic.

    I guess you didn’t read the comments I referenced by Allen. Here they are in entirety.

    from 5 years ago

    “Natural selection, though, adds no information. It only EVER reduces it. If you are trying to invoke mutations, then all known ones are (again) a loss of information.”

    This quote demonstrates a basic misunderstanding of the process of natural selection. According to Darwin (and virtually all evolutionary biologists), natural selection has three prerequisites:

    1) Variety (generated by the “engines of variation”

    2) Heredity (mediated by the transfer of genetic material, either vertically – from parents to offspring – or horizontally – via viral transduction, retrotranscription, etc.)

    3) Fecundity (reproduction, usually at a rate that exceeds replacement).

    Given these three prerequisites, the following outcome obtains:

    4) Demography: some individuals survive and reproduce more often than others. Ergo, the heritable variations of such individuals become more common over time in populations of those organisms.

    Natural selection is synonymous with #4; it is an outcome of the three processes listed first, not a “mechanism” in and of itself.

    Ergo, the real dispute here is not over natural selection per se, but rather the properties and capabilities of the “engines of variation”. I have written extensively about these here:

    http://evolutionlist.blogspot……ution.html

    and here:

    http://evolutionlist.blogspot……awman.html

    Yes, natural selection (i.e. #4, above) is conservative not creative. It produces no new genetic nor phenotypic information, which is why Darwin eventually came to prefer the term “natural preservation” rather than “natural selection”.

    However, it is also abundantly clear that the “engines of variation” – that is, the processes the produce phenotypic variation among the members of populations of living organisms – are both extraordinarily creative and extraordinarily fecund. The real problem in biology is not producing new variation, but rather limiting the production of new variation to the point that the “engines of variation” do not cause the rapid disintegration of living systems.

    As just one example of this problem, the genetic elements known as transposons generate a huge amount of new genetic variation, much of which is either phenotypically neutral or deleterious to the organism. There are biochemical mechanisms by which cells can monitor the incidence of transposition in themselves, and limit its consequences (up to and including the active self-destruction of the cell via apoptosis).

    At the same time, there is very good evidence in the genomes of many organisms that retrotransposition events mediated by transposons have produced genetic changes that have resulted in increased survival and reproduction of the organisms in which such events have taken place. There is a large and growing literature on this phenomenon, all of which points to the inference that retrotransposition via transposons both creates new genetic and phenotypic variation, and that in some cases such variation can provide the raw material for evolutionary adaptations, which are preserved via natural selection.

    So, if you really want to find out where the “intelligent designer” might create new variations, you should follow the lead of Darwin’s good friend, Asa Gray, and look for the telltale evidence for such intervention in the “engines of variation”. Of course, you will have to show pretty conclusively, using empirical investigations and statistical analysis, that such “creation events” are not the result of purely natural, unguided processes. If you can do this, you will undoubtedly win a Nobel Prize and a Crafoord Prize (plus a MacArthur or two).

    Notice that this will involve looking carefully into the mechanisms by which new variations are produced, rather than pointing to the outcomes of such processes (i.e. natural selection) and simply asserting that “you can’t get here from there”. Simply asserting (without empirical evidence) that something can’t happen isn’t “doing science” at all. In fact, it’s doing just the opposite…

    From last week

    Long repetitive sequences (LINEs and SINEs) clearly do not have a coding function, as they lack promoter sequences (which are absolutely necessary for a sequence to be transcribed and subsequently translated). However, they may have other biological functions. For example, the coding sequences in eukaryotic DNA are not entirely randomly located. Rather, they are located in parts of the genome that allow them to be associated with the histone proteins in nucleosomes. This is because modification of DNA binding to histones is an important mechanism of gene regulation in eukaryotes. Therefore, the “spacer” non-coding DNA such as LINEs and SINEs could still influence the expression of genes located at significant distances away by modifying their binding to histones in nucleosomes.

    As for the “engines of variation,” I would like to emphasize that the kind of variation I have written about is both genetic and phenotypic variation. Indeed, the majority of the mechanisms I listed in my “engines of variation” posts at The Evolution List are mechanisms that primarily affect gene expression, rather than gene sequence. Regulation of gene expression in eukaryotes is both complex and massive (I know, I’m teaching a course in it right now). Simply knowing the number of coding sequences in the genome of a multicellular eukaryote (especially an animal), for example by knowing the number and location of promoter sequences, tells you almost nothing about how the coding sequences (i.e. “genes”) are expressed and regulated. There are hierarchical biochemical systems involving anti-sense RNAs, small polypeptides, proteins, and non-coding sequences in DNA that all interact to produce the components of the phenotype. Increasingly fine-grained analyses of these systems has revealed that many of them are “kludges;” that is, they work, but not well and not always consistently. This “kludginess” of gene expression/regulation in eukaryotic cells is an apparently inescapable concomitant of both the complexity of the systems involved and the history of their implementation Think about how kludgy a huge OS like Windows has become; it’s essentially a small core of original integrated code, massively modified by an almost uncountable patchwork of “bug fixes” and “extensions.” The surprising thing about such systems is not that they don’t work well (they don’t), but rather that they work at all.

    It is becoming clear that the “software” of a typical eukaryotic cell is really mostly “kludgeware.” It generally works “just good enough” to not self-destruct. And, as it is replicated and modified (and especially as “foreign” sequences are introduced into it or removed from it by retrotranspositions, transposons, retroviral insertions, polymerase “skip-copying” and other “noise” events), it stumbles along in much the way that “Mendel’s Accountant” and the nearly-neutral theories predict that it should.

    This is one of the main reason that germ cells are set aside very early in embryonic development in eukaryotes. The less often the genome is replicated, the fewer mistakes it accumulates. This is part of what is wrong with “Mendel’s Accountant:” it doesn’t take into account the particular kinds of cells that actually constitute the ongoing phylogenetic lines it purports to describe. THe MA model assumes that all cells change randomly at approximately constant rates, yet germ cells don’t change at anything like the same rates as most cells, primarily because they don’t undergo mitotic divisions at anything like the rates of most other cells.

    And may I say that gpuccio is entirely correct about the idea that homologies (combined with shared derived sequences) are indeed very strong evidence for common descent. This is especially the case for non-coding sequences that have little or no effect on phenotypes. There are a multitude of examples of homologous sequences that either have no effect on phenotypes or have surprisingly different effects in different organisms as a result of modified gene expression in diverging phylogenetic lines. The assertion that the origin of such homologies is the result of the intervention of an intelligent designer, however, is not empirically verifiable or falsifiable, and so I won’t address it.

    As for how functional orphans can arise from non-coding sequences, one first has to specify what kind of non-coding sequences one is referring to. If one means LINEs and SINEs, then I agree completely. Transforming a very long sequences of repeated tandem repeats into a coding sequence, complete with a promoter, terminator, and enhancing sequences would indeed be miraculous. However, a significant fraction of the non-coding sequences in eukaryotes consist of sequences that were once viable coding sequences. These either were corrupted and thereby inactivated by mis-replication of their promoters/enhancers or (more commonly) were inserted into the genome as the result of retrotransposition, reverse transcription, transposon insertion, and similar processes, in which coding sequences with functional promoters, terminators, and enhancers are inserted or removed from the genome. In a great many cases, such sequences are quickly identified and inactivated by “surveillance/editing” mechanisms, which identify and inactivate the “rogue” sequences by inactivating their promoters and/or enhancers.

    However, this means that “dead” former coding sequences are scattered throughout the genome and can be reactivated by inserting new, active promoters/enhancers that can reactivate part or all of the “dead” sequences. This has actually been accomplished in the laboratory, where a “dead” retroviral sequence estimated at being inactive for millions of generations was “resurrected” by providing it with an active promoter sequence. The “fossil” sequence then acted like a functional virus, infecting host cells and generally acting like “its old (now extinct) self.”

    So, can reactivation of non-coding sequences produce new, functional gene sequences? Yes, if the non-coding sequences were once active coding sequences that had been inactivated by modification of their promoters/enhancers.

  29. 29
    jerry says:

    No, the whole debate is about what is the cause of design in nature/ biology

    This sounds like those who object to ID because we cannot identify the designer and how the designer did it.

    Before one can get to design, the EF requires one to eliminate natural origins of the entities. I just provided a way to do that which eliminates nearly every way the naturalist proposes. When these processes are eliminated, I am sure they will have new ones.

  30. 30
    scordova says:

    Cost of Maintenance: associated with Nachman’s Paradox and Poisson distributions as discussed in Fixation rate, what about breaking rate

    Cost of Construction: associated with Haldane’s Dilemma

    Larry and PZ’s solution, “molecular evolution is mostly free of selection, therefore no cost, evolution comes free of charge, what a deal!”

  31. 31
    Joe says:


    No, the whole debate is about what is the cause of design in nature/ biology

    This sounds like those who object to ID because we cannot identify the designer and how the designer did it.

    It does? In what way?

  32. 32
    Joe says:


    Really? Where are the testable hypotheses for blind and undirected processes producing genomes?

    They will be in the genomes of supposedly related species.

    That doesn’t even make any sense.

  33. 33
    Joe says:

    Jerry, Allen’s is not in any peer-review journal. As a matter of fact there isn’t any theory of evolution in a peer-review journal

  34. 34
    scordova says:

    Mr. Coder wrote:

    So much for “free peer review”.

    Well, let’s see what the reviewers have to say about this question:

    http://www.uncommondescent.com.....es-evolve/

  35. 35
    jerry says:

    It does? In what way?

    You said “No, the whole debate is about what is the cause of design in nature/ biology” I am not sure what this means because it is too vague or broad. But it sounds like those who object to ID because no one can point to a specific designer and what methods they used. They will say it is nature because there never was a designer. Richard Dawkins would except ID if there was someone who he could point to as long as it was not God.

    The debate has always been about the origin of new alleles. Meyer makes that point in his book but he use the term “information” which essentially means the same thing. Meyer goes on to point out that it is much more than alleles by talking about body plans but until now the debate was over new coding regions or alleles leading to proteins. This is what Axe and Durston’s work is all about, the impossibility of new alleles arising naturally.

    The debate is now expanding to the origin of regulatory system as well as coding regions or body plan information. Again the origin of new functional information.

  36. 36
    gpuccio says:

    jerry:

    In this thread:

    http://www.uncommondescent.com...../#comments

    Allen MacNeill posted at #100 what you quote at #28 here.

    I answered with some detail in post #111. He has not answered. You can give a look at my post, if you like.
    I remain of the same opinion.

  37. 37
    jerry says:

    I lost my internet connection. Have to use the 3G connection on my iPhone to read this.

    Gpuccio,

    I read your reply to Allen though on an iPhone it is difficult. Generally agree with all of it except I believe you are reading Allen a little wrong. This is a complicated issue. My connection just returned.

  38. 38
    jerry says:

    Really? Where are the testable hypotheses for blind and undirected processes producing genomes?

    I gave you the examples. People here tend to look at one side of the naturalist agenda and assume no other. They look at Darwinian gradualism and assume that is it. But there are others who publish and Allen MacNeill obviously has access to this type of thinking no matter what you personally think of him. Cornell is not some backwater university and he teaches evolutionary biology there and has a published course on evolution at the Modern Scholar. So he is knowledgeable.

    Those who defend the punctuated equilibrium scenario point to another origin of alleles. It is the slow mutation of non-coding, non functional regions of the genome. Various parts of this very large area is mutating away in all the individuals of a population and over time they claim that a new allele will arise. So essentially they are challenging Axe and Durston.

    And this is testable. If such a process is happening then it will arise throughout the species not just in one small sub-population. When a separated population develops the new allele, there will be parts of this coding sequence in other parts of the parent population. However, these sequences will not be functional. So for every unique coding sequence there will be evidence of it not succeeding in similar species.

    These make testable hypothesis.

  39. 39
    jerry says:

    I provided this reference before on how a segment of the evolutionary biologist think: It is an article by jurgen Brosius

    http://www.bioone.org/doi/abs/.....2.0.CO%3B2

    If you can get the Brosius article, read it. He certainly has a non Darwinian approach that is naturalistic.. It is in a journal titled, Paleobiology (Paleobiology 31(sp5):1-16. 2005 ).

    He was recommended by Allen MacNeill and it is about change in the non-functional DNA due to mutation. His ideas are testable and are opposed to Axe and Durston.

  40. 40
    gpuccio says:

    jerry:

    Unfortunately, I cannot get the article. The abstract, indeed, is not very informative, although I must say that the simple term “exaptation” is usually enough to make me mad.

    So, for the moment I will atick with Axe and Durston. 🙂

  41. 41
    Eric Anderson says:

    Can someone explain to me the important distinction between “exaptation” and “adaptation”?

    The explanation at the Berkeley website leaves a lot to be desired.

    http://evolution.berkeley.edu/.....ions.shtml

    They seem to focus on whether natural selection produced something for current function. (Certainly an unknowable, but let’s set aside that gaping problem for a moment).

    In contrast, exaptation (we are informed) is a result of things like “co-option”, and they use the term “co-option” as though it were a real process on its own separate from natural selection. What is co-option, if not another form of adaptation? How can co-option occur apart from natural selection? Does the feature just “poof” into its new role? Is not the feature maintained in that role after all by natural selection? If so, how does that role differ from natural selection’s role in any other situation?

    Sadly, I note that they also talk of natural selection “producing” new features, which of course it doesn’t.

    The whole “explanation” should drive any sane person to, if not downright reject the story, then at least toward some nagging doubts.

  42. 42
    Acartia_bogart says:

    Bornagain said “Acartia_bogart @2, perhaps you would like to tell us how Natural Selection, a process selecting 3-Dimensional phenotypes, produces 4-Dimensional systems?:”

    I must admit that I read your comment several times and still do not understand what you are trying to say. Which means that you must be s genius or an idiot. I won’t tell you which category I think you fall in.

  43. 43
    scordova says:

    So much for “free peer review”. Larry Moran is complaining about this blog post but doesn’t offer a counter-argument. Nor has anyone yet done so in the comments

    Larry may not be happy with the way I characterized his position, but he doesn’t seem to have much to criticize about my cost-of-selection argument. That’s what I was more interested in anyway.

  44. 44
    jerry says:

    Can someone explain to me the important distinction between “exaptation” and “adaptation”?

    I don’t know if I can but it may be worth while knowing what certain naturalists think.

    Here are Wikipedia’s definitions:

    An adaptation, also called an adaptive trait, in biology is a trait with a current functional role in the life history of an organism that is maintained and evolved by means of natural selection.

    I believe this means a pre-existing coding sequence has multiple alleles and will be subject to some mutations and the specific sequences that will survive will depend upon natural selection. The sequences or characteristics that survive will depend upon the particular environment the population is in.

    Exaptation (a replacement for the teleologically-loaded term “pre-adaptation”) and the related term co-option describe a shift in the function of a trait during evolution. For example, a trait can evolve because it served one particular function, but subsequently it may come to serve another.

    I believe this term applies to something that already exists and now has a different function. I believe one of the most famous recent examples is that part of flagellum is made up of parts that have other functions in different species. So a particular part was exapted to have a new use.

    If I am reading some of the Gould stuff correctly, it can also refer to a sequence that has no function but with a certain mutation can be functional. So mutation of non functional DNA can turn into functional DNA. This may be an example of exaptation too.

    Anyone else want to give it a shot.

  45. 45
    Eric Anderson says:

    Thanks, jerry, that is a valiant stab at it.

    If adaptation includes things that are “maintained and evolved by means of natural selection”, is then the proposal that exaptation did not involve natural selection or is not maintained by natural selection?

    The only way I can see that being true is if (i) they are admitting exaptation was pure dumb luck, a shot in the dark, or (ii) they are confused because they don’t understand natural selection well enough to describe it properly (the more likely scenario, in my view).

    One foundational problem with the description they offer is that if we look at an adaptive feature, such as echolocation (according to the Berkeley website), they are saying that it “evolved” by natural selection and that its function has always been echolocation. So if the parts of the echolocation mechanism didn’t serve some other function (as assumed), then they cannot have been built up slowly by natural selection. They must have come about by chance. All at once. Or by neutral theory, with no function at all, until one glorious day, Poof!, function burst onto the scene. In either case we are right back to Behe’s irreducible complexity argument.

    Part of the alleged power of co-option is that it gives the evolutionary story a back door through which it can claim an irreducibly complex structure came about, without relying on the Poof! theory. But if we are to eschew the Poof! theory, such co-opted parts must have evolved and been preserved by natural selection and the newly irreducibly complex structure must also be preserved by natural selection.

    At any rate, I would be very interested to know how anyone thinks exaptation works, if not, after all, through the magic of natural selection.

    And how do we properly distinguish a feature with “current” function (which is, of course, all we can actually observe) from one with a co-opted part that had prior function? The main time someone tried to do this — with the bacterial flagellum — they got egg on their face when it was shown that, if anything, the flagellum would have preceded the Type III secretory system. In any case, most co-option claims are simply another just-so story, supported by little more than a few comparative analyses and a healthy dose of imagination.

    It seems the only reasonable alternative is to treat exaptation as a sub-category of adaptation.

    Alternatively, I’d very much like to know, if not natural selection, what power or process causes a biological feature to take on another role and remain in that new role in an organism?

  46. 46
    Mung says:

    I like this simple definition:

    ex·ap·ta·tion (?g?z?p-t??sh?n)
    n. Biology
    The utilization of a structure or feature for a function other than that for which it was developed through natural selection.

  47. 47
    Eric Anderson says:

    Thanks, Mung. I needed that laugh. 🙂

    You’re probably right that this is about as good of a definition as we are likely to get.

    So we know that an existing observable feature was previously used for something else because . . . ?

    And we know that such a previously-useful structure came to be used for its new function without the involvement of natural selection because . . . ?

  48. 48
    AVS says:

    We know an existing feature was previously used for something else by looking at species who have evolved from a common ancestor and kept the original function. Take for example the appendix in humans vs. other mammals.
    That’s the beauty of evolution guys, it puts biology into context and connects all forms of life.

  49. 49
    JoeCoder says:

    AVS, are you sure the appendix is a good example for inferring common descent? I think it’s very much the opposite:

    the 50 species [with an appendix] are scattered so widely across the tree that the structure must have evolved independently at least 32 times, and perhaps as many as 38 times. … When just the clear-cut cases are included, the appendix evolved 18 times, he says.

  50. 50
    JoeCoder says:

    Or maybe you were joking. If so, apologies for my broken humor detection.

  51. 51
    AVS says:

    It represents a very good example of evolution. I’m not really sure how the article refutes that.

  52. 52
    Eric Anderson says:

    AVS @48:

    Here, let me fix it for you:

    “We know presume an existing feature was previously used for something else by looking at species who are presumed to have evolved from a common ancestor and kept the original function. And then we presume that the feature in one of the species represents the original function (i.e., we call that “adaptation”), and that the feature in the other species was not original (i.e., we call that “exaptation”).

    There, that is more accurate.

    Even then, it still doesn’t explain why someone would assert that exaptation came about and is preserved by something other than natural selection. What other force, pray tell, is there for evolution to turn to?

  53. 53
    AVS says:

    Thank you EA, although when we presume these things and they end up actually fitting together, evolution starts to make sense, no?
    I’m not sure what your problem is with exaptation being preserved by natural selection. The original function has been lost but there still is a minor function that benefits the organism, hence the organ remains.

  54. 54
    jerry says:

    I believe the term “exaptation” is also being used when a non functional coding sequence takes on function. That seems to be how Gould and Brosius used it to describe the origin of some novelties.

    they are confused because they don’t understand natural selection well enough to describe it properly

    I think they understand it ok. We tend to twist what it means and what it can do. See Allen MacNeill’s comment above which I posted. It is pretty clear.

    they are admitting exaptation was pure dumb luck, a shot in the dark,

    Yes, but there hundreds of trillions of shots in the dark and some of them hit a functional sequence. This is where there is a challenge to Axe and Durston.

    And why I say that these successful shots in the dark are in genomes of related species and why it is a testable hypothesis. It is just a matter of getting enough genomes sequenced and compared to see how the successful shot in the dark arose. It has to leave a forensic trail. Of course if the forensic evidence is not there, then how did the coding sequence arise. Axe and Durston salt it cannot arise by chance.

    t seems the only reasonable alternative is to treat exaptation as a sub-category of adaptation.

    IMaybe for some of the examples. But for where a novel sequence suddenly becomes functional, that is not really adaption. Only in the sense that the novel sequence coded a new protein which somehow now affected survival.

    Alternatively, I’d very much like to know, if not natural selection, what power or process causes a biological feature to take on another role and remain in that new role in an organism?

    Unknown I guess. But a lot of non-coding sequences get transcribed and I guess it can then get translated and if it produces a viable protein, the organism may then use it somehow. Seems very iffy.

    Also a lot of the changes between species are not in the coding sequences but in the regulatory sequences and in the epigenetic elements. They are only just beginning to touch all of this. A vast new area is ahead. Whether any random process can explain it is unknown.

  55. 55
    Eric Anderson says:

    AVS @53:

    Thank you EA, although when we presume these things and they end up actually fitting together, evolution starts to make sense, no?

    Yes, if we presume the very issues that need to be demonstrated then we can easily fall into the trap of thinking it all fits together nicely. But it is just in our minds, and not necessarily based on observed reality.

    gpuccio noted a similar slip into circular thinking here:

    http://www.uncommondescent.com.....ent-497267

    I’m not sure what your problem is with exaptation being preserved by natural selection. The original function has been lost but there still is a minor function that benefits the organism, hence the organ remains.

    I don’t have a problem with natural selection being involved in exaptation. Indeed, it seems it must be. That is why several of the definitions seem to be flawed, including the one at the Berkeley website I linked to.

  56. 56
    AVS says:

    Not based on observed reality? I guess you’re not familiar with the field of evolutionary biology…
    Do you not realize that there are thousands of scientists out there in the field right now, studying evoltuion? That for the last hundred years we have slowly proven evolution to be the most likely explanation for the diversity of species we see today? This is all based on studies done that test the reality of nature.
    I’m not sure how the definition is flawed there.

  57. 57
    Eric Anderson says:

    Thanks, jerry.

    I think they understand it ok. We tend to twist what it means and what it can do.

    Sorry, but when we have people talking about natural selection (see the Berkeley website) as though it “produces” new features, then either (i) they don’t know what they are talking about, or (ii) they don’t know how to explain it properly.

    Yes, but there hundreds of trillions of shots in the dark and some of them hit a functional sequence.

    Maybe. That is the real question, isn’t it? Can random shot-in-the-dark changes in a nucleotide sequence stumble upon a functional sequence that actually can be utilized in a cell in the real world? And if so, how often can this be expected to occur?

    But for where a novel sequence suddenly becomes functional, that is not really adaption. Only in the sense that the novel sequence coded a new protein which somehow now affected survival.

    Isn’t that how all sequences allegedly arose? They weren’t functional at some point; then they were. And somehow they affected survival.

    It doesn’t sound much different from the general description of how adaptations arise: mutations and various other random changes take place, some of them aid survival and stick.

    But a lot of non-coding sequences get transcribed and I guess it can then get translated and if it produces a viable protein, the organism may then use it somehow. Seems very iffy.

    Yes, quite iffy. Furthermore, if the sequence didn’t do anything beforehand then — by the very definitions we have been seeing on this thread — we can’t be dealing with exaptation, because exaptation (we are told) requires that the trait had some different, prior function.

    —–

    Look, at the end of the day the whole theory boils down to: “Random stuff happens. Some of it works and gets preserved.”

    I’m just tired of people using fancy terms like “co-option” and “exaptation” as though they are providing an explanation for what actually goes on, as though such terms provide some additional useful understanding. Most of the time they don’t. Many people see the fancy terms, assume the scientist must know what he is talking about, and back off. I tend to be less impressed, particularly if they can’t provide any substance behind the fancy terms. It is so often just smoke and mirrors. Often not even intentionally; in some cases they are just throwing out the best ideas they have.

    The alleged explanations underlying the theory, amusingly and ironically, often mirror the theory’s main alleged mechanism — a shot in the dark.

  58. 58
    AVS says:

    This phrase of yours EA, makes me think you have a misunderstanding about exaptation;
    “Alternatively, I’d very much like to know, if not natural selection, what power or process causes a biological feature to take on another role and remain in that new role in an organism?”
    Natural selection is involved in exaptation as far as I can tell,and the Berkeley site does not say different.
    I think I know where your making a mistake. Try reading that first sentence of the definition of exaptation again, and this time do not stop after the words “natural selection.” Read the last four words also. They are a very important part of the definition.

    You guys didn’t do very well with the whole “reading comprehension” thing in school did you?

  59. 59
    jerry says:

    Eric,

    We tend to talk about only one type of naturalist view of evolution here. I assume you brought up the term exaptation because it was in the title of the Brosius article. It was in a book titled “Macroevolution” by Vrba and Eldredge who were colleagues of Stephen Gould.

    The article is extremely technical. They do not deny natural selection or gradualism in some senses but only that traditional Darwinian thought cannot explain a lot of evolution. That is why the term exaptation is a big deal to them. They are trying to explain the sudden appearance of novelty.

    Gradualism in the Darwinian sense won’t do it so exaptation is invoked. This allows them to use currently available elements and rearrange them and get something brand new and to use formerly non-functional parts of the genome and use it to get something new. Both are sudden events, not gradual ones.

    So I would look to Gould and his colleagues to see what they have/are saying. Allen MacNeill obviously includes their ideas in his thinking and is why he said Neo Darwinian was dead but he did not say naturalism was dead. He subscribes to a New Synthesis.

    I personally believe the New Synthesis suffers the same problem the whole one did, namely, a lack or probable resources to accomplish anything of meaning. But the interesting thing is all these ideas are now testable and will be in the next 10 years or so as new genomes get analyzed.

  60. 60
    jerry says:

    Last comment: should be in last paragraph:

    I personally believe the New Synthesis suffers the same problem the old one did.

  61. 61
    Eric Anderson says:

    AVS:

    I realize you jumped into the middle of the discussion and may not be aware of the nuance that is being discussed.

    The following series of questions will help pinpoint the issue:

    1. Why is exaptation not considered an adaptation under some definitions? Is it better to think of exaptation as a subcategory of adaptation?

    2.a. How do we know that our alleged “adaptation” didn’t have a prior function? And if the system in question had no prior function, is that an acknowledgement that the entire function — with all its integrated parts and complexities — burst onto the scene at once? What about the “slight, successive” development concept at the heart of the natural selection story?

    2.b. How do we know that our alleged “exaptation” had a prior different function? (This point we have touched on briefly earlier in the thread.)

    3. If a feature was “co-opted” for its current use from a prior use, is that not an example of natural selection in action? If so, then this situation would seem to be picked up by the definition of “adaptation” jerry cited from Wikipedia. Yet, the Berkeley website informs us that exaptation is not an adaptation.*

    These are some of the nuances I am interested in exploring. This is not a battle for sledgehammers, but for scalpels. Indeed, it need not even be a battle, so there is no need to make it so.

    —–

    *The Wikipedia definition appears superior, on logical grounds, to the Berkeley definition, though the latter implies it is based on Gould’s and Vrba’s definitions, which I would think we should be hesitant to jettison without good reason.

  62. 62
    Eric Anderson says:

    jerry @59:

    Thanks for your thoughtful comments.

    They do not deny natural selection or gradualism in some senses but only that traditional Darwinian thought cannot explain a lot of evolution. That is why the term exaptation is a big deal to them. They are trying to explain the sudden appearance of novelty.

    Gradualism in the Darwinian sense won’t do it so exaptation is invoked. This allows them to use currently available elements and rearrange them and get something brand new and to use formerly non-functional parts of the genome and use it to get something new. Both are sudden events, not gradual ones.

    Thanks, this is helpful. It confirms part of what I suspected. It essentially functions in an analogous fashion to the “punctuated equilibrium” idea — large scale changes happening quickly in geological time (without, we might be forgiven for noticing, any sound mechanism to explain how it could in fact happen).

    It is noteworthy (as it was with punctuated equilibrium) that we have large-scale acknowledgement that “slight, successive” changes + natural selection won’t cut it in so many cases. Good to keep in mind.

    I personally believe the New Synthesis suffers the same problem the whole one did, namely, a lack or probable resources to accomplish anything of meaning. But the interesting thing is all these ideas are now testable and will be in the next 10 years or so as new genomes get analyzed.

    Agreed on the lack of resources to accomplish anything interesting.

    I’m skeptical, however, that comparative genomics can tell us as much as you seem to think they can. At the risk of belaboring the thread longer, I would be genuinely interested in your thoughts as to how comparative genomics will resolve the issue?

    Thanks,

  63. 63
    gpuccio says:

    Eric:

    I agree with jerry that comparative genomics can answer many things. Among them:

    a) Confirm that there is no evidence at all of selectable intermediates to basic protein domains.

    b) Confirm that there is no evidence of exaptation as a general mechanism to generate functional information.

    c) Confirm the existing evidence for new functional proteins arising from non translated sequences, without any possible interventions of NS.

    And, probably, many other things.

    All these things point to design.

    I would add that comparative transcriptomics can be even more important.

  64. 64
    Eric Anderson says:

    Thanks, gpuccio. That is a good starting list.

    Don’t get me wrong. There is value in comparative research and an honest researcher will be able to learn many interesting things and, no doubt, a few important things. There will be new lines of argumentation open up for the design proponent as more and more biology research is done.

    As far as it impacts the design/evolution debate, however, I don’t think it will make much of an impact. Let’s take your first example:

    Let’s assume that after exhaustive research it is indeed confirmed, and recognized by all, that there is no evidence of selectable intermediates to basic protein domains.

    What will be the evolutionary response? They will not say, “OK, we were wrong.” No. There are two arguments that will be made:

    1. There were intermediates, but they were lost over time. This is basically the same situation we have with the fossil record. Only this time with molecular “missing links.”

    or

    2. “We don’t need no stinkin’ intermediates!” In other words, the argument will be that evolution was able — somehow — to do what it did without molecular intermediates.

    So, just as similarities in sequences cannot prove hereditary descent, dissimilarities cannot prove the lack thereof.

    Already today, without breaking a sweat and without invoking any comparative genomics, we could come up with a hundred examples of things in biology that scream design and that would cause any reasonable person to doubt the efficacy of blind, unguided evolution.

    However, for the committed evolutionist, certainly for the committed materialist, all these examples are not seen as evidence against evolution. Rather, they are seen just as another confirmation of the wonderful things evolution can produce. Hearts, lungs, wings, eyes, digital coding systems — isn’t it amazing what evolution can produce!

    Anything from comparative genomics that demonstrates the lack of viable mechanisms for evolutionary processes will just be met with claims that either (i) the mechanism was there at one time, but has been lost over time, or (ii) evolution really didn’t need that mechanism after all.

  65. 65
    AVS says:

    My only point, EA, was to correct you on your interpretation of the berkeley website’s definition of exaptation.

  66. 66
    gpuccio says:

    Eric:

    I agree with you: nothing can work against dogma.

    But we must think of science, and believe that reason and good faith will prevail sooner or later.

    In the meantime, refining our knowledge and our understanding can only help.

    As I said in another post, the real purpose is not to win on Moran, AVS and their similars, but to understand truth.

  67. 67
    AVS says:

    And the truth is poochy, that there is a mountain of evidence that suggests evolution is the explanation for the diversity of species we see today. We just don’t entirely understand the process, as it is very complex and requires knowledge that we don’t have yet.

  68. 68
    gpuccio says:

    AVS:

    I say it again. The purpose is not to win on you.

  69. 69
    AVS says:

    I was just curious what you’d say, I couldn’t remember if you were the one here that played both sides of the fence and believed in “designed evolution” or some such.
    Just me fishing.

  70. 70
    Eric Anderson says:

    AVS

    My only point, EA, was to correct you on your interpretation of the berkeley website’s definition of exaptation.

    That may have been your intent, but it was based on a misunderstanding on your part, not mine. I have not misinterpreted the words on the Berkeley website. The issue related to a nuance that, until now, it is clear you hadn’t before considered.

    Now that you are presumably up to speed on what we are talking about, perhaps you’d like to enlighten us as to whether exaptation is a form of adaptation (as could arguably be the case under the Wikipedia definition) or whether it is not an adaptation (as per the Berkeley website)?

  71. 71
    AVS says:

    You have to think in terms of function and time.

    It seems an adaptation represents the original function that arose through natural selection, whereas an exaptation is a secondary function that arose due simply to the presence of the original adaptation. The role of natural selection in an exaptation seems to be only in maintaining the function, which was what I was trying to point out to you originally.

    I think the feathers example works quite well here.

  72. 72
    jerry says:

    Eric,

    I came across a useful set of videos on genetics. If you or anyone are interested, go to youtube and search for “useful genetics.” There is a series of lectures, some short, some about 20 minutes. The author is a colorful person in more ways than one. Check out the hair over time.

    https://www.youtube.com/user/UsefulGenetics

    One particularly interesting one is the comparison of genomes. It is lecture 1G. Lecture 1H is about human differences and the so called our of Africa scenario. Another is 2b which breaks down the genome by the various parts and it is obvious that the coding region is a very small part of the genome. By viewing this we would all be on the same page on just what is in the genome.

    As far as testing for naturalistic changes, any change must have left a trail in the genome in successes as well as failures. By analyzing the failures as well as the successes one can determine if the new sequences arose by natural means.

    If any changes took place gradually and failed to take place in a sister species, it will be visible in the comparative genomes. Otherwise it will have to have appeared suddenly with no genetic precursors. These sequence take tens of million of years to develop so the sub-population will be very similar to the related species except it will have one or more sequences that are functional but are very similar to the other species but are not functional in that related species.

    Maybe that can be expressed clearer but it has to be true if any naturalist theory is true. I suspect we will not find this almost homologous sequence in other species which means it arose on its own and that is probability impossible. Genomes are getting very cheap to sequence and it is just a matter of time before the analysis is done.

  73. 73
    jerry says:

    Eric and gpuccio,

    If you do not read this, I will post it again when it is appropriate

    I was able to get a pdf of the Brosius article I referred to above. In this and other articles, he cites chapter and verse on how genes arise. Here are a couple of excerpts from this article that show how they think:

    An extension of Wally Gilbert’s metaphor “exons in a sea of introns” (Gilbert 1978). Functional nuons are is lands in a sea of nonfunctional (nonaptive) sequences. Nevertheless, any of those sequences has the potential to be exapted into novel functions (Brosius and Gould 1992; Balakirev and Ayala 2003). While “plate tectonics,” or exon shuffling, occasionally leads to rearrange ments of existing functional nuons (Gilbert 1978), retro position, the major force in the plasticity of genomes, which in our analogy is more akin to volcanic eruptions, frequently creates new nuons. Initially, most nuons (is lands) are barren (nonfunctional, nonaptive) but have the potential to be fertilized by some microevolutionary base changes or short indels and exapted as functional nuons. Nonfunctional nuons erode over time and the is lands disappear in the sea of anonymous sequences. An interesting example is the recruitment of part of an Alu retronuon as an alternative exon in an isoform of the cytokine tumor necrosis factor receptor. Insertion of the Alu element occurred after Anthropoidea split from pro simians and a subsequent point mutation generated an ATG start codon. This base substitution alone, however, was not sufficient for exaptation of the Alu element as a protein-coding exon, as this sequence is nonaptive (not used as part of an alternative mRNA) in Platyrrhini. Only two additional small changes in the lineage lead ing to Catarrhini including apes, a C->T transition to generate a GT 5′ splice site and a 7-bp deletion to pro vide translation into the next exon in the correct reading frame, led to generation and exaptation of this alternative exon (Singer et al. 2004).

    A nuon is any distinct nucleic acid, a defined sequence module (Brosius and Gould 1992). The term can be used with a prefix (e.g., retronuon) to designate any DNA module that was generated by retroposition. I prefer retronuon over retroposon and especially over transposable element (TE) or mobile element (ME). In fact, any RNA is a potential mobile element: if a segment of the genome is transcribed in the germline it has the potential to serve as template for retroposition (hence, RNA might be considered the ultimate selfish unit). However, upon integration into the genome, there is no guarantee for autonomous transcription in the germline, which results in a loss of mobility. The original transcript, how ever, can serve as a template for retroposition multiple times. In contrast to TE or ME, the term “retronuon” solely indicates the mode of origin, but not the potential for successive amplification. Only a minority of retronuons are true TEs or MEs, such as endogenous retroviruses or intact LINE elements [see Brosius 2003a]).

    An online previous study by Brosius and Gould is here

    http://www.pnas.org/content/89/22/10706.full.pdf

    The abstract

    ABSTRACT Genomic nomenclature has not kept pace with the levels and depth of analyzing and understanding genomic struure, function, and evolution. We wish to propose a general terminology that might aid the integrated study of evolution and molecular biology. Here we designate as a “nuon” any stretch of nucleic acid sequence that may be identifiable by any critenon. We show how such a general term will facilitate contemplation of the structural and functional contributions of such elements to the genome in its past, current, or future state. We focus in this paper on pseudogenes and dispersed repetitive elements, since their current names reflect the prevalent view that they constitute dispensable genomic noise (trash), rather than a vast repertoire of sequences with the capacity to shape an organism during evolution. This potential to contribute sequences for future use is reflected in the suggested terms “polonuons” or “pologenes.” If such a potonuon has been coopted into a variant or novel function, an evolutionary process termed “exaltation,” we employ the term “xaptonuon.” If a potonuon remains without function (nonaptive nuon), it is a “nonaptation” and we term it “naptonuon.” A number of examples for potonuons and xaptonuons are given.

    Another of Brosius’ articles

    http://zmbe.uni-muenster.de/ex.....o.2003.pdf

    The abstract

    Retroposition is an ancient process dating back to the conversion of RNA to DNA genomes. Nevertheless, it continues to make tremendous structural and functional contributions to extant genomes. This process and the endurance, or even renaissance, of an RNA world in many lineages sheds a new light on the Central Dogma of Molecular Biology. The question of why reverse ranscriptase has survived billions of years without an apparent cellular function is discussed. Retroposition constitutes one of the pervasive conflicts, in this case between host genome on one hand and mobile genetic elements on the other, that fuel the evolutionary process. It is obvious that retroposition has, thus far, contributed numerous useful novelties to genomes.

    A recent article

    http://gbe.oxfordjournals.org/...../2061.full

    The abstract

    The evolution of new genes can ensue through either gene duplication and the neofunctionalization of one of the copies or the formation of a de novo gene from hitherto nonfunctional, neutrally evolving intergenic or intronic genomic sequences. Only very rarely are entire genes created de novo. Mostly, nonfunctional sequences are coopted as novel parts of existing genes, such as in the process of exonization whereby introns become exons through changes in splicing. Here, we report a case in which a novel nonprotein coding RNA evolved by intron-sequence recruitment into its structure. cDNAs derived from rat brain small RNAs, revealed a novel small nucleolar RNA (snoRNA) originating from one of the Snord115 copies in the rat Prader–Willi syndrome locus. We suggest that a single-point substitution in the Snord115 region led to the expression of a longer snoRNA variant, designated as L-Snord115. Cell culture and footprinting experiments confirmed that a single nucleotide substitution at Snord115 position 67 destabilized the kink-turn motif within the canonical snoRNA, while distal intronic sequences provided an alternate D-box region. The exapted sequence displays putative base pairing to 28S rRNA and mRNA targets.

    For all of Brosius’ articles

    http://zmbe.uni-muenster.de/in.....AllPub.pdf

    The people at UD have to be aware of people like Brosius. He is not the stereotype of people like Coyne, Moran and Dawkins that are characterized here on UD.

  74. 74
    Joe says:

    AVS:

    And the truth is poochy, that there is a mountain of evidence that suggests evolution is the explanation for the diversity of species we see today.

    Only if it started with a huge diversity, including metazoans.

    BTW there still isn’t any eviodence for natural selection actually doing something

  75. 75
    gpuccio says:

    jerry:

    I am absolutely convinced that transposons are a powerful tool for gene design. They model functional sequences from non coding sequences. Intelligently. I have defended that model of “guided mutation as an implementation of design” many times here. And transposons are the most likely implementation tool, at present.

    The simple fact is: if transposons (or any other mechanism) acted randomly, they would just be a variant of random variation, and they could never generate complex functional information, as they seem to do.

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