Evolution Genetics Genomics

Many genes relatively new, scientists find

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Science writer Carl Zimmer in the New York Times on recent discoveries in the ongoing evolution of genes:

New genes were long thought to derive from duplications or mistakes in older genes. But small mutations can also form new genes from scratch.

For some scientists, like Dr. Tautz, the data pointed to an inescapable conclusion: Orphan genes had not been passed down through the generations for billions of years. They had come into existence much later.

“It’s almost like Sherlock Holmes,” said Dr. Tautz, citing the detective’s famous dictum: “When you have eliminated the impossible, whatever remains, however improbable, must be the truth.”

Dr. Begun and his colleagues renamed orphan genes “de novo genes,” from the Latin for new. He found that many of his fellow scientists weren’t ready to accept this idea.

Can’t think why not, can you? 😉

While many de novo genes ultimately vanish, some cling to existence and take on essential jobs. Dr. Tautz said the rise of these genes might be as important a factor in evolution as gene duplication.

Now how will this affect attempts to construct evolutionary histories via genome mapping?

More Zimmer on the genome:

One gets the impression that the guy who thought our genomes were in some sense “us” spoke too quickly.

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182 Replies to “Many genes relatively new, scientists find

  1. 1
    Jehu says:

    “It’s almost like Sherlock Holmes,” said Dr. Tautz, citing the detective’s famous dictum: “When you have eliminated the impossible, whatever remains, however improbable, must be the truth.”

    so when we have eliminated random chance … ?

  2. 2
    ppolish says:

    Creation is such a fascinating aspect of Evolution – from origins of lifes to de novo genes popping into existence as we speak.

    It truly needs it’s own field within Evolution study. Maybe call it Creation Science?

  3. 3
    ppolish says:

    Creation is such a fascinating aspect of Evolution – from origins of lifes to de novo genes popping into existence as we speak.

    It truly needs it’s own field within Evolution study. Maybe call it Creation Science?

  4. 4
    jw777 says:

    This seems like a very Johnny-come-lately “revelation.” Genes aren’t that important in our understanding of “us”ness anymore, so much so to the point where terms like membranome have to be coined.

  5. 5
    bornagain77 says:

    as to the this claim

    “New genes were long thought to derive from duplications or mistakes in older genes. But small mutations can also form new genes from scratch.”

    The trouble with this line of thought (‘just so story’) from Darwinists, besides the fact that the origin of a new gene has never been observed in the lab,(Behe; First Rule), is that many orphan genes are expressed early in embryonic development:

    Age doesn’t matter: New genes are as essential as ancient ones – December 2010
    Excerpt: “A new gene is as essential as any other gene; the importance of a gene is independent of its age,” said Manyuan Long, PhD, Professor of Ecology & Evolution and senior author of the paper. “New genes are no longer just vinegar, they are now equally likely to be butter and bread. We were shocked.”
    http://www.sciencedaily.com/re.....142523.htm

    New genes in Drosophila quickly become essential. – December 2010
    Excerpt: The proportion of genes that are essential is similar in every evolutionary age group that we examined. Under constitutive silencing of these young essential genes, lethality was high in the pupal (later) stage and (but was) also found in the larval (early) stages.
    http://www.sciencemag.org/cont.....2.abstract

    Yet mutations expressed early in embryonic development are ‘always catastrophically bad’:

    A Listener’s Guide to the Meyer-Marshall Debate: Focus on the Origin of Information Question -Casey Luskin – December 4, 2013
    Excerpt: “There is always an observable consequence if a dGRN (developmental gene regulatory network) subcircuit is interrupted. Since these consequences are always catastrophically bad, flexibility is minimal, and since the subcircuits are all interconnected, the whole network partakes of the quality that there is only one way for things to work. And indeed the embryos of each species develop in only one way.” –
    Eric Davidson
    http://www.evolutionnews.org/2.....79811.html

    Darwin or Design? – Paul Nelson at Saddleback Church – Nov. 2012 – ontogenetic depth (excellent update) – video
    Text from one of the Saddleback slides:
    1. Animal body plans are built in each generation by a stepwise process, from the fertilized egg to the many cells of the adult. The earliest stages in this process determine what follows.
    2. Thus, to change — that is, to evolve — any body plan, mutations expressed early in development must occur, be viable, and be stably transmitted to offspring.
    3. But such early-acting mutations of global effect are those least likely to be tolerated by the embryo.
    Losses of structures are the only exception to this otherwise universal generalization about animal development and evolution. Many species will tolerate phenotypic losses if their local (environmental) circumstances are favorable. Hence island or cave fauna often lose (for instance) wings or eyes.
    http://www.saddleback.com/mc/m/7ece8/

    Understanding Ontogenetic Depth, Part II: Natural Selection Is a Harsh Mistress – Paul Nelson – April 7, 2011
    Excerpt: The problem may be summarized as follows:
    — There are striking differences in the early (embryonic) development in animals, even within classes and orders.
    — Assuming that these animals are descended from a common ancestor, these divergences suggest that early development evolves relatively easily.
    — Evolution by natural selection requires heritable variation.
    — But heritable variations in early development, in major features such as cleavage patterns, are not observed.
    http://www.evolutionnews.org/2.....45581.html

    Moreover, Gene Regulatory Networks are not reducible DNA sequences

    Gene Regulatory Networks in Embryos Depend on Pre-existing Spatial Coordinates – Jonathan Wells – July 2011
    Excerpt: The development of metazoan embryos requires the precise spatial deployment of specific cellular functions. This deployment depends on gene regulatory networks (GRNs), which operate downstream of initial spatial inputs (E. H. Davidson, Nature 468 [2010]: 911). Those initial inputs depend, in turn, on pre-existing spatial coordinate systems. In Drosophila oocytes, for example, spatial localization of the earliest-acting elements of the maternal GRN (Gene Regulatory Network) depends on the prior establishment of an anteroposterior body axis by antecedent asymmetries in the ovary. Those asymmetries appear to depend on cytoskeletal and membrane patterns rather than on DNA sequences,,,
    http://www.discovery.org/scrip.....38;id=7751

    Moreover, Genetic Regulatory Networks between Chimps and Humans ‘differ by orders of magnitude’:

    “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
    http://www.metacafe.com/watch/8593991/

    Evolution by Splicing – Comparing gene transcripts from different species reveals surprising splicing diversity. – Ruth Williams – December 20, 2012
    Excerpt: A major question in vertebrate evolutionary biology is “how do physical and behavioral differences arise if we have a very similar set of genes to that of the mouse, chicken, or frog?”,,,
    A commonly discussed mechanism was variable levels of gene expression, but both Blencowe and Chris Burge,,, found that gene expression is relatively conserved among species.
    On the other hand, the papers show that most alternative splicing events differ widely between even closely related species. “The alternative splicing patterns are very different even between humans and chimpanzees,” said Blencowe.,,,
    http://www.the-scientist.com/?.....plicing%2F

  6. 6
    bornagain77 says:

    Moreover, it turns out that Darwinism can’t explain optimization of any useful kind:

    Oxford University Admits Darwinism’s Shaky Math Foundation – May 2011
    Excerpt: However, mathematical population geneticists mainly deny that natural selection leads to optimization of any useful kind. This fifty-year old schism is intellectually damaging in itself, and has prevented improvements in our concept of what fitness is. – On a 2011 Job Description for a Mathematician, at Oxford, to ‘fix’ the persistent mathematical problems with neo-Darwinism within two years.
    http://www.evolutionnews.org/2.....46351.html

    Yet embryonic development is found to be optimal:

    Seeing the Natural World With a Physicist’s Lens – November 2010
    Excerpt: Scientists have identified and mathematically anatomized an array of cases where optimization has left its fastidious mark, among them;,, the precision response in a fruit fly embryo to contouring molecules that help distinguish tail from head;,,, In each instance, biophysicists have calculated, the system couldn’t get faster, more sensitive or more efficient without first relocating to an alternate universe with alternate physical constants.
    http://www.nytimes.com/2010/11.....038;st=cse

    Development of a fly embryo in real time – video
    http://www.youtube.com/watch?v=OQ86d9sTeaQ

    Of related interest:

    Alexander Tsiaras: Conception to birth — visualized – video
    http://www.youtube.com/watch?v=fKyljukBE70
    Comment on preceding video: Mathematician and medical image maker Alexander Tsiaras offers a stunning visualization of the process that in nine months takes an emerging human life from conception to birth. He speaks of “the marvel of this information,” “the mathematical models of how these things are done are beyond human comprehension,” “even though I look at this with the eyes of mathematician I look at this and marvel. How do these instruction sets not make mistakes as they build what is us?”

    An Electric Face: A Rendering Worth a Thousand Falsifications – September 2011
    https://www.youtube.com/watch?v=0VULjzX__OM

    Symphony of Life, Revealed: New Imaging Technique Captures Vibrations of Proteins, Tiny Motions Critical to Human Life – Jan. 16, 2014
    Excerpt: To observe the protein vibrations, Markelz’ team relied on an interesting characteristic of proteins: The fact that they vibrate at the same frequency as the light they absorb.
    This is analogous to the way wine glasses tremble and shatter when a singer hits exactly the right note. Markelz explained: Wine glasses vibrate because they are absorbing the energy of sound waves, and the shape of a glass determines what pitches of sound it can absorb. Similarly, proteins with different structures will absorb and vibrate in response to light of different frequencies.
    http://www.sciencedaily.com/re.....084838.htm

    Verse and Music:

    Psalm 139:15
    My frame was not hidden from You, When I was made in secret, And skillfully wrought in the depths of the earth;

    Mercyme – All Of Creation –
    http://www.youtube.com/watch?v=kkdniYsUrM8

  7. 7
    Mung says:

    But when scientists gained the ability to sequence entire genomes, there was a surprise waiting for them. They started to find genes that existed in the genome of just one species. According to the duplication theory, these solitary genes shouldn’t exist; they would have to have been copied from earlier genes in other organisms.
    Continue reading the main story

    “They looked like perfectly normal genes, except they were only found in one species,” said Anne-Ruxandra Carvunis, an evolutionary biologist at the University of California, San Diego. “There was no explanation for how a gene could be in one species and not in other ones.”

    These genes came to be known as “orphan genes.”

    Dr. Begun and his colleagues renamed orphan genes “de novo genes,” from the Latin for new. …

    Some clues come from diseases. Japanese researchers, for example, have found a de novo gene involved in cancer. The gene, called NCYM, is found only in humans and chimpanzees, suggesting that it arose several million years ago in our common ancestor.

    Are humans and chimpanzees the same species? If not, is NCYM really an orphan gene?

  8. 8
    Mung says:

    …genomic studies are now turning up hundreds of thousands of genes in many diverse organisms that exhibit no significant similarity in sequence to any other known gene. These “taxonomically restricted genes” or “ORFans” (for “open reading frames of unknown origin”) now dot the phylogenetic landscape. Darwin’s Doubt p.215-216

    I have a question for those Young Earth Creationists who believe that ORFan’s are your friends. How many fruit fly “kinds” did God create when he created the kinds, or do you believe that God created each individual species of fruit fly as a separate “kind”?

    How do young earth creationists explain ORFan genes?

  9. 9
    Piotr says:

    Are humans and chimpanzees the same species? If not, is NCYM really an orphan gene?

    It arose as a de novo gene in the common ancestor of humans and chimps. It’s significant that we have such an new gene in common with chimps rather than, say, with macaques to the exclusion of the big apes. Like ERVs, such newly acquired genes follow a pattern reflecting the nested hierarchy of relatedness.

  10. 10
    Joe says:

    Another evo that doesn’t understand nested hierarchies. Priceless.

    ERVs- nope- they ain’t ERVs just alleged remnants that “look like” parts of ERVs.

  11. 11
    Joe says:

    Mung- YECs explain ORFan genes by way of non-random evolution, ie “built-in responses to environmental cues” (Spetner 1997).

    IOW no need to create all species of fruit flies- just one population with the information required for adaptations is all that is required.

  12. 12
    Piotr says:

    Another evo that doesn’t understand nested hierarchies. Priceless.

    Here’s a YEC who thinks he understands them…

    ERVs- nope- they ain’t ERVs just alleged remnants that “look like” parts of ERVs.

    … and who doesn’t know the definition of “ERV”.

  13. 13
    Joe says:

    What YEC, Piotr? And I know what an ERV is. Your false accusations just prove you are an ass on an agenda.

    BTW in EVERY case I had an argument with evos on nested hierarchies I have been the only one to provide references to support my claims.

  14. 14
    bornagain77 says:

    Piotr, it is funny that Darwinists are quick to point to any similarity that makes it seem there theory is plausible, but they are completely blind to any differences that render any Darwinian explanation void of power.,,,

    For instance, so great are the anatomical differences between humans and chimps that a Darwinist actually proposed that a chimp and pig mated with each other and that is what ultimately gave rise to humans:

    A chimp-pig hybrid origin for humans? – July 3, 2013
    Excerpt: Dr. Eugene McCarthy,, has amassed an impressive body of evidence suggesting that human origins can be best explained by hybridization between pigs and chimpanzees. Extraordinary theories require extraordinary evidence and McCarthy does not disappoint. Rather than relying on genetic sequence comparisons, he instead offers extensive anatomical comparisons, each of which may be individually assailable, but startling when taken together.,,,
    The list of anatomical specializations we may have gained from porcine philandering is too long to detail here. Suffice it to say, similarities in the face, skin and organ microstructure alone is hard to explain away. A short list of differential features, for example, would include, multipyramidal kidney structure, presence of dermal melanocytes, melanoma, absence of a primate baculum (penis bone), surface lipid and carbohydrate composition of cell membranes, vocal cord structure, laryngeal sacs, diverticuli of the fetal stomach, intestinal “valves of Kerkring,” heart chamber symmetry, skin and cranial vasculature and method of cooling, and tooth structure. Other features occasionally seen in humans, like bicornuate uteruses and supernumerary nipples, would also be difficult to incorporate into a purely primate tree.
    http://phys.org/news/2013-07-c.....umans.html

    Moreover, Physorg published a subsequent article showing that the pig-chimp hybrid theory for human origins is much harder to shoot down than Darwinists had first supposed it would be:

    Human hybrids: a closer look at the theory and evidence – July 25, 2013
    Excerpt: There was considerable fallout, both positive and negative, from our first story covering the radical pig-chimp hybrid theory put forth by Dr. Eugene McCarthy,,,By and large, those coming out against the theory had surprisingly little science to offer in their sometimes personal attacks against McCarthy.
    ,,,Under the alternative hypothesis (humans are not pig-chimp hybrids), the assumption is that humans and chimpanzees are equally distant from pigs. You would therefore expect chimp traits not seen in humans to be present in pigs at about the same rate as are human traits not found in chimps. However, when he searched the literature for traits that distinguish humans and chimps, and compiled a lengthy list of such traits, he found that it was always humans who were similar to pigs with respect to these traits. This finding is inconsistent with the possibility that humans are not pig-chimp hybrids, that is, it rejects that hypothesis.,,,
    http://phys.org/news/2013-07-h.....dence.html

    The obvious question for me is, of course, since Darwinists are having such a hard time proving that we did not come from pig-chimp hybrids, what makes Darwinists so sure that we evolved from apes or anything else in the first place? Any reasonable person would realize that if such a dubious theory as the pig-chimp hybrid theory can cause such havoc, for what was suppose to be such well established science, then perhaps the Darwinian theory for human origins is not nearly as strong as Darwinists have dogmatically held it to be in the first place. Some might even hold that such ‘flimsiness’ would clearly indicate the original theory was rubbish as to being hard science.

    supplemental note:

    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

    Human Origins(?) by Brian Thomas, M.S. – December 20, 2013
    Excerpt: Three major pillars supporting a human-chimp link crashed in 2013.
    1. Genetic similarity (70% instead of 98%)
    2. beta-globin pseudogene (functional instead of leftover junk)
    3. Chromosome 2 fusion site (encodes a functional feature within an important gene instead of a being a fusion site) All three key genetic pillars of human evolution (for Darwinists) turned out to be specious—overstatements based on ignorance of genetic function.
    http://www.icr.org/article/7867/

  15. 15
    Piotr says:

    What YEC, Piotr?

    Glad to know that you aren’t. So what’s the age of the Earth and of its biosphere, in your opinion?

    And I know what an ERV is. Your false accusations just prove you are an ass on an agenda.

    For the record: you are already calling me names. I won’t imitate your manners — anybody can see who’s a real ass anyway. Your comment above shows that you have a problem with the definition. You say:

    ERVs- nope- they ain’t ERVs just alleged remnants that “look like” parts of ERVs.

    Well, for your education, that’s precisely what ERVs are by definition: remnants of proviruses integrated into the genome. They resemble viral genomes and are derived from them. In your comment you confuse ERVs with active retroviruses.

    BTW in EVERY case I had an argument with evos on nested hierarchies I have been the only one to provide references to support my claims.

    Jolly good joke, Joe.

  16. 16
    bornagain77 says:

    Piotr you claim,,,

    They (ERVs) resemble viral genomes and are derived from them.

    Yet your claim is not nearly as strong as you seem to think:

    Refutation Of Endogenous Retrovirus – ERVs – Richard Sternberg, PhD Evolutionary Biology – video
    http://www.youtube.com/watch?v=SrEOe2E0Euc
    Sternberg, R. v. & J. A. Shapiro (2005). How repeated retroelements format genome function. Cytogenet. Genome Res. 110: 108-116.

    Endogenous retroviruses regulate periimplantation placental growth and differentiation – 2006
    http://www.pnas.org/content/103/39/14390.abstract.

    Retrovirus in the Human Genome Is Active in Pluripotent Stem Cells – Jan. 23, 2013
    Excerpt: “What we’ve observed is that a group of endogenous retroviruses called HERV-H is extremely busy in human embryonic stem cells,” said Jeremy Luban, MD, the David L. Freelander Memorial Professor in HIV/AIDS Research, professor of molecular medicine and lead author of the study. “In fact, HERV-H is one of the most abundantly expressed genes in pluripotent stem cells and it isn’t found in any other cell types.
    http://www.sciencedaily.com/re.....133930.htm

    Transposable Elements Reveal a Stem Cell Specific Class of Long Noncoding RNAs – (Nov. 26, 2012)
    Excerpt: The study published by Rinn and Kelley finds a striking affinity for a class of hopping genes known as endogenous retroviruses, or ERVs, to land in lincRNAs. The study finds that ERVs are not only enriched in lincRNAs, but also often sit at the start of the gene in an orientation to promote transcription. Perhaps more intriguingly, lincRNAs containing an ERV family known as HERVH correlated with expression in stem cells relative to dozens of other tested tissues and cells. According to Rinn, “This strongly suggests that ERV transposition in the genome may have given rise to stem cell-specific lincRNAs. The observation that HERVHs landed at the start of dozens of lincRNAs was almost chilling; that this appears to impart a stem cell-specific expression pattern was simply stunning!”
    http://www.sciencedaily.com/re.....192838.htm

    Retroviruses and Common Descent: And Why I Don’t Buy It – September 2011
    Excerpt: If it is the case, as has been suggested by some, that these HERVs are an integral part of the functional genome, then one might expect to discover species-specific commonality and discontinuity. And this is indeed the case.
    http://www.uncommondescent.com.....nt-buy-it/

    The definitive response on ERV’s and Creation, with Dr. Jean Lightner
    http://www.youtube.com/watch?v=feHYEgzaGkY

    etc.. etc…

    as with the claims made by Darwinists, ERVs appear to be overstatements based on ignorance of genetic function.

    Of course it would be good if Darwinists ever got to the business of science and ever actually demonstrated the feasibility of their claims instead of just claiming that Darwinian evolution is the way all life happened and never demonstrating that it is feasible:

    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 (>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

    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.
    http://www.discovery.org/a/9461

  17. 17
    Piotr says:

    @B77 (I’ll ignore the irrelevant parts)

    Being derived from a provirus doesn’t mean the the ERV sequence can’t be co-opted for some useful function, though most of them are not recycled in that way and evolve neutrally. But we were talking about the pattern of their occurrence. Do you know examples of orthologous ERVs that occur in humans and baboons but not in chimps or gorillas?

  18. 18
    Jehu says:

    Mung,

    How do young earth creationists explain ORFan genes?

    You are kidding right? Creationists explain ORFans easily. They were created by God.

  19. 19
    Jehu says:

    Piotr

    Do you know examples of orthologous ERVs that occur in humans and baboons but not in chimps or gorillas?

    Your question assumes common descent.

  20. 20
    Jehu says:

    Ptior,

    I think the proper creationist answer would be, there are no orthologous genes outside of a baramin (created kind).

  21. 21
    bornagain77 says:

    Piotr you state:

    I’ll ignore the irrelevant parts

    Funny that the ‘irrelevant parts’ you chose to ignore have to do exactly with seeing whether or not Darwinian evolution is even feasible in reality,,,

    When Theory Trumps Observation: Responding to Charles Marshall’s Review of Darwin’s Doubt -Stephen C. Meyer – October 2, 2013
    Excerpt: Developmental gene regulatory networks (dGRN) are control systems. A labile (flexible) dGRN would generate (uncontrolled) variable outputs, precisely the opposite of what a functional control system does. It is telling that although many evolutionary theorists (like Marshall) have speculated about early labile dGRNs, no one has ever described such a network in any functional detail — and for good reason. No developing animal that biologists have observed exhibits the kind of labile developmental gene regulatory network that the evolution of new body plans requires. Indeed, Eric Davidson, when discussing hypothetical labile dGRNs, acknowledges that we are speculating “where no modern dGRN provides a model” since they “must have differed in fundamental respects from those now being unraveled in our laboratories.”8
    By ignoring this evidence, Marshall and other defenders of evolutionary theory reverse the epistemological priority of the historical scientific method as pioneered by Charles Lyell, Charles Darwin and others.9 Rather than treating our present experimentally based knowledge as the key to evaluating the plausibility of theories about the past, Marshall uses an evolutionary assumption about what must have happened in the past (transmutation) to justify disregarding experimental observations of what does, and does not, occur in biological systems. The requirements of evolutionary doctrine thus trump our observations about how nature and living organisms actually behave. What we know best from observation takes a back seat to prior beliefs about how life must have arisen.
    http://www.evolutionnews.org/2.....77391.html

    How convenient that you choose to ignore observational evidence in favor of speculative evidence that must be shoehorned!

    of note:

    cases of anomalous ERVs
    http://www.uncommondescent.com.....ent-449621

    The Human Lineage Was Somehow “Purged” – Cornelius Hunter – April 2012
    Excerpt: Another such feature is the lack of endemic infectious retroviruses in humans. The problem is that these viruses are present in the other primates, and so according to evolutionists these viruses must be present in their common ancestor which, again according to evolution, would be an ancestor of humans as well.,, In other words, when evolution spontaneously created humans our DNA must have been “purged.” We got a do-over! Hilarious.
    http://darwins-god.blogspot.co.....-free.html

    etc.. etc..

  22. 22
    bornagain77 says:

    Piotr, it might also interest you to know that ‘form’ is not even reducible to DNA sequences as is presupposed in the reductive materialism of neo-Darwinism:

    Laszlo Bencze: So evolution is a poor at predicting results? – April 29, 2014
    Excerpt: recent studies have shown that species which look very similar and behave similarly can have vastly different genetic structure (notably frogs). In other words the genetic studies do not accord with studies based on phenotype. So much for certainty.
    http://www.uncommondescent.com.....g-results/

    Family Ties: Completion of Zebrafish Reference Genome Yields Strong Comparisons With Human Genome – Apr. 17, 2013
    Excerpt: Researchers demonstrate today that 70 per cent of protein-coding human genes are related to genes found in the zebrafish,,,
    http://www.sciencedaily.com/re.....131725.htm

    Shark and human proteins “stunningly similar”; shark closer to human than to zebrafish – December 9, 2013
    Excerpt: “We were very surprised to find, that for many categories of proteins, sharks share more similarities with humans than zebrafish,” Stanhope said. “Although sharks and bony fishes are not closely related, they are nonetheless both fish … while mammals have very different anatomies and physiologies.
    http://www.uncommondescent.com.....zebrafish/

    Kangaroo genes close to humans
    Excerpt: Australia’s kangaroos are genetically similar to humans,,, “There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order,” ,,,”We thought they’d be completely scrambled, but they’re not. There is great chunks of the human genome which is sitting right there in the kangaroo genome,”
    http://www.reuters.com/article.....P020081118

  23. 23
    Joe says:

    Piotr:

    So what’s the age of the Earth and of its biosphere, in your opinion?

    No one knows. You have to know how the earth was formed in order to determine its age and no one knows that.

    Well, for your education, that’s precisely what ERVs are by definition: remnants of proviruses integrated into the genome.

    And yet a retrovirus isn’t a remnant and there isn’t anything in the word “endogenous” that makes it so. Is an exogenous virus also just remnants then?

    So you must be talking about EVEs- endogenous viral elements.

    REgardless, there isn’t any way to test the claim that Common Descent produced thge pattern observed. And there isn’t any way to test the claim that a virus was the sole cause of the alleged remnants.

    As for nested hierarchies, no joke, it is a fact that I can support. Ya see Piotr evos think that any branching pattern is a nested hierarchy. They also think that descent with modification produces a nested hierarchy. Both are false.

    Just because a nested hierarchy can be depicted using a branching pattern does not mean all branching patterns are a nested hierarchy. Nested hiwerarchies need to exhibit summativity- For example the Animal Kingdom is the sum of al of the sets and levels below it, ie the sum of all the animals.

    Genes and EVEs do not exhibit summativity but they can be placed in a branching pattern

  24. 24
    Piotr says:

    @Joe

    Why don’t you just check the standard definitions of ERV and EVE?

    https://en.wikipedia.org/wiki/Paleovirology

    Note that every ERV is an EVE but there are also other types of EVEs.

    @Jehu

    I think the proper creationist answer would be, there are no orthologous genes outside of a baramin (created kind).

    But baramins are just compartments. They don’t form a hierarchy, so you can’t account for the hierarchical patterns in the distribution of ERVs etc. with their help.

  25. 25
    Joe says:

    Piotr- Can an ERV be an active whole virus? Yes or no

  26. 26
    Piotr says:

    A freshly integrated ERV can be a complete provirus (the genome of a retrovirus). It can even retain some activity, though it doesn’t seem to be true of the known human ERVs, which are all defective at present.

  27. 27
    Joe says:

    Thank you. When you mentined ERVs above you were just talking about remnants, correct? Are ERVs the only explanation for the remnants of ERV-like DNA?

  28. 28
    Joe says:

    Piotr- baramins form a nested hierarchy. Linnean classification is a nested hierarchy- guess what it was based on? The common design of the Created Kinds

  29. 29
    Joe says:

    Piotr 15:

    Well, for your education, that’s precisely what ERVs are by definition: remnants of proviruses integrated into the genome.

    Piotr 26

    A freshly integrated ERV can be a complete provirus (the genome of a retrovirus).

    So, for my education, an ERV can refer to remnants or entire proviruses. That means, in context, my statement in 10 is not wrong at all.

  30. 30
    Piotr says:

    That means, in context, my statement in 10 is not wrong at all.

    You said: “they ain’t ERVs” (correcting what I’d said). That was wrong: they are ERVs, and there was nothing to correct in the first place.

  31. 31
    Piotr says:

    baramins form a nested hierarchy. Linnean classification is a nested hierarchy- guess what it was based on? The common design of the Created Kinds

    Please explain the method of design, and why the result looks for all the world as if it were produced by common descent (including features that evolve neutrally and have no identifiable function, like those defunct and decaying ERV sequences). A conspiracy? A prankster god?

    You know, Linnaeus correctly recognised cetaceans as mammals but he would never have dreamt of placing them inside Artiodactyla (since he was working with limited data). Now we have both fossil and molecular evidence that they are a branch of artiodactyls. Why did God give the various artiodactyls (pigs, giraffes, deer, sheep, buffaloes, etc., and cetaceans) a common set of features only to give a few more just to cetaceans and hippos, and then some more exclusively to Cetacea (“un-designing” their hind legs, hair, and a few other things at the same time)? What motivated such a strange plan of design?

  32. 32
    Mung says:

    Piotr:

    It arose as a de novo gene in the common ancestor of humans and chimps.

    So is it incorrect to say that ORFan genes are found only in a single species?

    “There was no explanation for how a gene could be in one species and not in other ones.”

    These genes came to be known as “orphan genes.”

    What is the difference between an ORFan gene and a taxonomically restricted gene, if any?

    If so, many of these new genes would likely be taxonomically restricted genes (TRGs), orphan sequences not found outside a species or only found in a particular taxonomic group
    here

    We suggest that orphans should now be classified as ‘taxonomically restricted genes’ (TRGs), as this concept seems more useful for advancing our knowledge of these sequences and their potential ecological significance.
    here

    Here we focus on evidence from Hydra suggesting that taxonomically-restricted genes play a role in the creation of phylum-specific novelties such as cnidocytes, in the generation of morphological diversity, and in the innate defence system. We propose that taxon-specific genes drive morphological specification, enabling organisms to adapt to changing conditions.
    here

  33. 33
    Mung says:

    Mung:

    How do young earth creationists explain ORFan genes?

    Joe:

    YECs explain ORFan genes by way of non-random evolution, ie “built-in responses to environmental cues” (Spetner 1997).

    Hi Joe, there’s no entry in the index to Spetner’s book for ORFan gene, orphan gene, species-specific gene or taxonomically restricted gene. I’ll re-read the chapter on non-random variation.

    Jehu:

    You are kidding right? Creationists explain ORFans easily. They were created by God.

    No I’m not kidding. I’d like to know. Some YEC’s seem to think they are evidence for young earth creationism and I’d like to know how and why they come to that conclusion.

    So far I asked the question and received two very different answers.

    Most YEC’s, afiak, don’t think God is still creating new species. You seem to be one who does. Do you believe God is still creating new species and that’s why ORFan genes arise?

    Or is are they a result of evolution, like Joe says, just not random evolution?

    Some YEC’s are anti-evolution, others accept evolution within kinds. I am just trying to figure it all out so I can understand how ORFan genes support young earth creationism (if at all).

  34. 34
    Mung says:

    Jehu:

    I think the proper creationist answer would be, there are no orthologous genes outside of a baramin (created kind).

    So do YEC’s use orphan genes to help determine the created kinds? Do you have any references? If so, how do they support young earth creationism?

  35. 35
    Mung says:

    Hi Piotr,

    I don’t recall is interacting before. Hope you’ll stick around. What’s your interest in ID?

  36. 36
    Jehu says:

    Mung,

    So do YEC’s use orphan genes to help determine the created kinds? Do you have any references? If so, how do they support young earth creationism?

    Orphans are inconsistent with common descent but consistent with created kinds. I don’t know if anybody has done a study of orphans as they relate to baraminology.

  37. 37
    Joe says:

    Piotr:

    That was wrong: they are ERVs, and there was nothing to correct in the first place.

    They just look like ERVs- remnants of ERVs.

    Please explain the method of design, and why the result looks for all the world as if it were produced by common descent (including features that evolve neutrally and have no identifiable function, like those defunct and decaying ERV sequences).

    I don’t know the method of design and the result doesn’t look as if it were produced by common descent. You don’t even know what pattern universal common descent would produce.

  38. 38
    Joe says:

    Mung:

    Hi Joe, there’s no entry in the index to Spetner’s book for ORFan gene, orphan gene, species-specific gene or taxonomically restricted gene. I’ll re-read the chapter on non-random variation.

    So you can’t put 2 and 2 together? 🙂 What part of “built-in responses to environmental cues” can’t produce ORFan genes?

  39. 39
    Mung says:

    Joe:

    What part of “built-in responses to environmental cues” can’t produce ORFan genes?

    Spetner:

    The system turns genes ON or OFF as they are needed, but makes no permanent change in the genome.

    – p. 182

    Does that answer your question?

  40. 40
    Mung says:

    Jehu:

    Orphans are inconsistent with common descent but consistent with created kinds.

    Why? How? And SO?

    My point is that if one is going to state or imply that ORFan genes support young earth creationism that an actual argument needs to be put forth.

    Why aren’t ORFan genes consistent with Old Earth Creationism?

    How are ORFan genes “consistent with created kinds” if they appear within different “kinds” of created kinds?

    Do ORFan genes require God’s direct intervention? If so, why? If not, why not?

    Is God still creating new species? If so, why is God not still creating new “kinds”?

  41. 41
    Piotr says:

    Mung: I don’t recall is interacting before. Hope you’ll stick around. What’s your interest in ID?

    I often lurk here out of curiosity. Nice talking to you guys. You can guess we disagree about most of this stuff, but I promise to be civil and patient.

  42. 42
    gpuccio says:

    Mung:

    A few tentative answers from my point of view.

    De novo genes appear throughout the course of natural history. In a strict sense, we call them ORFans if they remain restricted to one species or group of species.

    But, in another sense, each new protein superfamily (at least) is a de novo gene when it appears for the first time, even if after it remains common to many species which appear after.

    Each de novo gene, if functional and complex, requires the active intervention of a designer for its first appearance.

    There is increasing evidence that at least some de novo genes arise gradually from non coding sequences, without any possible intervention of NS, from a process which can only be explained as guided intelligent variation. We will see if that evidence is confirmed and validated by new data.

    There is no special reason to believe that the process has stopped.

  43. 43
    gpuccio says:

    Piotr:

    I have appreciated your interventions. You seem a reasonable interlocutor, a precious thing indeed.

    I am curious: what is your personal idea about the appearance of complex functional de novo genes, especially from non coding sequences?

  44. 44
    gpuccio says:

    Mung:

    I agree that the “turning of genes ON or OFF as they are needed” is an important mechanism of environmental adaptation, probably epigenetic, but sometimes due to simple genetic variation, and has nothing to do with the appearance of new complex functional genes.

    Many so called examples of “darwinian evolution” are of that kind, including the appearance of nylonase and the famous case of citrate in Lenski’s experiment. In those two cases, the “adaptation” is genetic, and could be explained as the result or simple random variation + NS (but it could still be algorithmic in some way).

    In other cases, the adaptation is probably due to the working of intelligent epigenetic algorithms.

  45. 45
    Piotr says:

    I am curious: what is your personal idea about the appearance of complex functional de novo genes, especially from non coding sequences?

    I don’t know enough about biochemistry to offer an original personal idea. Here’s my tuppenceworth based on what I’ve read: the accidental formation of a new “RNA gene”, complete with regulatory elements, is not at all unlikely. Again, in most cases it will be non-coding RNA which may or may not become co-opted for doing something useful. In extremely rare cases it may be translated into a protein (short, simple and relatively unstructured in the case of young genes, which doesn’t rule out certain kinds of functionality).

    If any of those products (non-coding RNA or peptide) confers an appreciable advantage, positive selection will eventually conserve it, so it may gradually develop into something more complex and more functional, or even give rise to a new gene family. If it turns out to be deleterious, purifying selection will prevent its spread. It may also evolve neutrally or nearly neutrally (not everything that regularly gets transcribed has a function).

  46. 46
    Joe says:

    Mung, Nice quote mine of Spetner. The part you quoted has nothing to do with what I am saying. Spetner also talks about long term changes, Mung.

    It’s as if y6ou have turned into an evo

  47. 47
    Piotr says:

    So is it incorrect to say that ORFan genes are found only in a single species?

    It doesn’t matter from the evolutionary perspective. You may replace ‘species’ with ‘lineage’ or ‘clade’. Here’s Tautz & Domazet-Lošo’s definition:

    Genes that lack homologues in other lineages — that is, they cannot be linked by overall similarity or shared domains to genes or gene families known from other organisms.

    It doesn’t say that an orphan gene must be restricted to one species (only of the youngest orphan genes will be; some may even be restricted to populations within a species). Large and old taxa also have genes with no external homologues (200+ in primates, including humans). The term “taxonomically restricted gene” (TRG) is used of them, and at least in some cases it can be demonstrated that they are old “orphan genes”. As in the case or ERVs, those that we share with e.g. baboons are a subset of those we share with gibbons, and these in turn are a subset of those shared with chimps/bonobos.

  48. 48
    Joe says:

    Piotr, How was it determined that the ORFan genes arose by accident? My bet it was just a bald declaration, no science involved

  49. 49
    Joe says:

    Piotr, Again with the ERVs that no one knows if they were ERVs. “It looks like part of an ERV to me” is not science.

  50. 50
    Joe says:

    There isn’t enough time for the blind watchmaker to A) duplicate a gene and B) have that gene changed for a different function and expressed.

    As Lenski has demonstrated duplicate genes do not necessarily, contra Art Hunt, have their promoters and binding sites duplicated.

  51. 51
    gpuccio says:

    Piotr:

    Thank you for the kind answer.

    Of course you have read those things. That is standard darwinist propaganda. Unfortunately, nothing of that is true or supported by facts.

    However, you certainly believe those things in good faith. I can only encourage you to read more, and with a critical spirit. Read also something specific of what is posted here, especially the more technical interventions.

    If you are interested, you could look at my recent posts here:

    http://www.uncommondescent.com.....modern-one

    for example, #57 and following (it’s a long discussion with rhampton7)

  52. 52
    gpuccio says:

    Joe:

    Piotr, How was it determined that the ORFan genes arose by accident? My bet it was just a bald declaration, no science involved

    It’s a good bet. You would certainly win. 🙂

    The simple facts are that we can observe some non coidng regions becoming functional ORFs at a certain point of natural history, if that will be confirmed.

    That is against all probabilistic considerations. Unless, obviously, the evolution of the sequence is intelligently guided.

    Usually, the non coding region becomes an ORF when it is ready to be translated, and to express the function. Until then, NS can act in no way, and only pure chance or design can be responsible.

    What would you bet on? 🙂

  53. 53
    Piotr says:

    @Joe

    The null hypothesis about the origin of de novo genes in this case is the random generation of transcribed sequences that accidentally acquire a function, since it makes no arbitrary assumptions and is compatible with known facts (see the article I linked). I invite you to falsify the null hypothesis and propose a more convincing scenario. For example, if you could show me a young orphan gene that encodes for a large and highly complex multi-domain protein involved in some really important interactions, I’d agree that the spontaneous rise of such a structure by accident is not a satisfactory explanation.

  54. 54
    Piotr says:

    gpuccio: Of course you have read those things. That is standard darwinist propaganda. Unfortunately, nothing of that is true or supported by facts.

    Shall I stop taking you seriously before we actually discuss anything? Read what you’ve just written. I gave you a link to a review article by highly respected experts on orphan genes, published in one of the best science journals, and you dismiss it off-hand as “darwinist propaganda” and a rigmarole of lies.

    Does it ever occur to you that if it weren’t for people who do actual scientific research and write such stuff, you (I mean ID proponents) would not even know of orphan genes and their functions? How can you, on the one hand, call someone’s results not true and unsupported by facts, and at the same time hijack them for your own purposes? It simply makes no sense.

    I am not a biochemist, but I am an academic worker engaged in research. I can tell science from propaganda, and I detect more of the latter in your three sentences above (note, for example, the agitprop application of the term “darwinist”) than in the article in question.

  55. 55
    Joe says:

    Piotr:

    The null hypothesis about the origin of de novo genes in this case is the random generation of transcribed sequences that accidentally acquire a function, since it makes no arbitrary assumptions and is compatible with known facts (see the article I linked).

    I invite you to test that null hypothesis. I also invite you to produce a testable model based on it.

    If you either cannot or refuse to we will understand why.

  56. 56
    Joe says:

    Piotr:

    I can tell science from propaganda

    Doubtful.

  57. 57
    Piotr says:

    The null hypothesis is the default position. You can reject it (or fail to reject it) if you propose an alternative hypothesis making more specific assertions, suggested by the data. I have offered one way in which you could disprove the “random origin” scenario. It predicts that the transcripts young de novo genes will be relatively short, yielding simple products like non-coding RNAs of small proteins. It makes other predictions too, e.g. that de novo genes will be cis-regulated rather than trans-regulated, that they will have few if any paralogues, etc. Go ahead, falsify it.

  58. 58
    Joe says:

    The null still needs to be tested. If it cannot be tested then it is rejected.

    The point being is there isn’t any reason to falsify something tat cannot be tested in the first place.

    It’s as if you have no clue wrt science.

  59. 59
    Joe says:

    Piotr:

    It predicts that the transcripts young de novo genes will be relatively short, yielding simple products like non-coding RNAs of small proteins. It makes other predictions too, e.g. that de novo genes will be cis-regulated rather than trans-regulated, that they will have few if any paralogues, etc.

    It predicts that just cuz you say so? You realize that you actually have to have some evidence as to why blind watchmaker evolution predicts that.

  60. 60
    Piotr says:

    @Joe:

    Of course it is testable. Are you suffing from a reading comprehension problem? How many times shall I repeat that I have suggested a way to test it? The evidence so far is compatible with “random origin”, so the hypothesis stands unfalsified. Now if you think you have some evidence of special design in orphan genes (using my suggestion or anything else), why don’t you present it, Mr Scientific? If you just keep repeating the same thing, I’ll ignore you henceforth.

  61. 61
    Piotr says:

    It predicts that just cuz you say so?

    No, the predictions aren’t mine. They follow from the model, but in order to understand how and why you’d have to do some reading, and I suspect you can’t be bothered.

  62. 62
    Joe says:

    Piotr, The designers and builders we know of do so one piece at a time. IOW your “predictions” are pure nonsense wrt random origins. No one in ID would expect a new gene in one generation.

    Also yours has the issue of once you have a functioning short protein there isn’t any known mechanism for adding to that sequence in such a way as to produce a totally new function with a longer chain. Not only that once you get to long chains (AA-wise) a chaperone is required in order to get a proper functioning fold.

    As for gene duplication there just isn’t enough time for accidental genetic changes to duplicate a gene, build a binding site and alter it in such a way as to change the function.

    The whole issue boils down to the origin of life. It is only if life arose via accidents and chance events would infer evolution is so driven. OTOH if the OoL was designed then we would infer that it was designed to evolve and evolved by design.

  63. 63
    Piotr says:

    Also yours has the issue of once you have a functioning short protein there isn’t any known mechanism for adding to that sequence in such a way as to produce a totally new function with a longer chain.

    If you mean that there is no such mechanism known to you, I’m prepared to believe you. Perhaps hou’ve never heard of domain duplication, insertion, gene fusion, recruitment of transposable elements, etc.

    All that stuff, however, is beside the point. The issue at hand is not what happens to orphan genes and their products once they arise and start evolving, but whether they can arise by chance in the first place. Duplication, let alone the origin of life, are separate topics. We are talking about the origin of orphan genes at the moment, so please let’s stay focussed.

    Have you got a creationist/designist explanation of the fact that orphan genes in humans (similarly to those in other species) don’t encode for complex proteins, that they are all single-copy genes, and that despite being specifically human, they correspond to non-translatable orthologous sequences in chimps and orangutans? Why should the designer have limited her creative freedom in this way?

  64. 64
    Upright BiPed says:

    Hello Piotr

    The issue at hand is not what happens to orphan genes and their products once they arise and start evolving, but whether they can arise by chance in the first place.

    They can’t “arise and evolve” without the irreducible complex system that precedes them.

    Duplication, let alone the origin of life, are separate topics.

    If it is argued by materialists that a life can be fully explained by unguided material processes (as is the case) … yet unguided material processes cannot explain the material conditions required for life to exist – then it is not a wholly “separate topic”.

    If materialists would like to reformulate their public proclamations that life is the result of a purely unguided material process, and amend it to say that there are important observations within the evolution of life that are explicable by purely material means – then we (generally, as a group) would have no problem with that position. It is the same one that ID proponents hold.

    We are talking about the origin of orphan genes at the moment, so please let’s stay focussed.

    If you are sensing resistance, perhaps you should realize that most ID proponents understand this to be a cop out. You are here clearly arguing that life is the product of materialial processes. So the obligatory “Let’s not talk about the evidence that materialism fails to address” is hardly sufficient to the ultimate question you are attempting to support.

    Obviously, there is nothing improper about limiting a discussion to a particular topic. There are many here that can (and will) address the mechanism(s) of the origin of orphan genes. Perhaps it would serve your purposes better to not merely say that the origin of living systems is simply “a separate topic”, but to acknowledge the evidence of design regarding origins, and its potential implications in the topic you wish to discuss.

    Such balance and discipline has appeared on these pages before, and typically results in a much more fruitful conversation.

  65. 65
    Piotr says:

    Upright Biped: They can’t “arise and evolve” without the irreducible complex system that precedes them.

    Still, the topic under discussion is the origin of orphan genes themselves, not the prehistory of the whole milieu in which they exist (or the origin of life, or the origin of the Universe, or my world-outlook). I’m willing to discuss anything on suitable occasions, but I prefer to stay focussed especially if straying off topic could be employed as an evasive tactic.

  66. 66
    Upright BiPed says:

    Piotr,

    I prefer to stay focussed especially if straying off topic could be employed as an evasive tactic.

    Well that’s exactly the point, I was making. The origin of the system that you take for granted in order to make your case is not off topic if your professed conclusion is that life is the result of a purely material process. Life is wholly dependent on an irreducibly complex system that cannot come into being by a stepwise process. Life is either the product of an inconceivable miracle of chance, or it is designed. And while the evidence surrounding a chance origin is less than zero, the physical evidence leading to a designed origin is both intractable and universal.

    If you are expecting ID proponents to ignore this fact so that our opponents aren’t bothered by it, then you simply ask too much – certainly more than you are willing to give.

  67. 67
    gpuccio says:

    Piotr:

    Shall I stop taking you seriously before we actually discuss anything?

    Your choice.

    I gave you a link to a review article by highly respected experts on orphan genes, published in one of the best science journals, and you dismiss it off-hand as “darwinist propaganda” and a rigmarole of lies.

    First of all, I already knew that paper.

    Second, my comment about the propaganda was mainly referred to your statements, rather than specifically to that paper.

    Third, that paper contains however a lot of darwinist propaganda, especially in the section “Emergence of protein structure”, even if it is expressed with some cautious intelligence.

    Fourth, the fact that researchers can do good work and be “highly respected experts” in their field is not in discussion, and has almost nothing to do with what we are discussing here. My point here, the point of many in ID, is that our scientific community has been experiencing a strong cognitive bias, in the last decades, in favor of a theory completely unsupported by facts, and logically inconsistent. This is a confrontation of paradigms, not of individuals.

    So, I will not accept anything here because of authority, not even from my side.

    And what are the “lies” you refer to?

    I stated:

    “Unfortunately, nothing of that is true or supported by facts.”

    I was referring to the following statements made by you:

    a) “the accidental formation of a new “RNA gene”, complete with regulatory elements, is not at all unlikely.”

    Based on what facts? That new genes (DNA genes I suppose, but transcribed) happens? Of course it happens. That is obvious. And where is the evidence that it is “accidental”? The whole point of ID is that functional genes cannot emerge by chance.

    And even if transcribed genes emerged by chance, they still would not be translated, and therefore would not be visible by NS.

    Where are the evidences that cells are repleted with non functional transcribed and translated genes, on whom NS can act? They are nowhere to be seen.

    b) “Again, in most cases it will be non-coding RNA which may or may not become co-opted for doing something useful.”.

    Based on what? Again, I agree that new genes come often from non coding DNA, but how does that DNA become apt to be “co-opted”, IOWs functional, against all probabilistic laws? No facts, no consistency.

    c) “In extremely rare cases it may be translated into a protein (short, simple and relatively unstructured in the case of young genes, which doesn’t rule out certain kinds of functionality).”

    Again, where are the facts that support this bizarre statements? This is complete mythology.

    Then I stated “However, you certainly believe those things in good faith.”, which I hope is not a lie, and gave you a link to some posts of mine which go in greater details.

    Where is the “rigmarole of lies”?

    Finally, I use propaganda to mean exactly that: propaganda. Concepts enforced to defend a wrong theory, without any rational and empirical support, are propaganda in my world.

    And I use the term “darwinism” for brevity, usually meaning neo darwinism, the modern synthesis, classical darwinism a la Dawkins. No agit prop application at all. When I want to be more precise, I refer in general to “non design theories of biological information”.

    I have been debating here for years the scientific reasons why none of those theories makes sense. I have given you a link to more detailed posts of mine. I don’t think it is fair on your part to label me in ways that have nothing to do with what I defend here. But again, it is your choice.

    Then I find this bizarre statement:

    “How can you, on the one hand, call someone’s results not true and unsupported by facts, and at the same time hijack them for your own purposes? It simply makes no sense.”

    I hate to remind you that there is a great difference between facts and their interpretation, in science. I appreciate facts, and those researchers who provide good facts. I feel in no way obliged to share their interpretation of those facts, if I believe that it is biased or simply wrong. Hijacking facts is a crime, now? Are you really serious?

    In another post, you say:

    “The null hypothesis is the default position. ”

    No. There is no “default” position in science. The null hypothesis is the hypothesis that the observed effect is due to chance. It is considered only to the purpose that its probability may be assessed. It’s that probability which will tell us if it is reasonable or not to reject the null hypothesis.

    You may be aware that neo darwinism avoids accurately the computation of real probabilities. That is the weapon of ID.

    Well, you should be satisfied. Now you can stop taking me seriously after I have actually discussed something. 🙂

  68. 68
    Joe says:

    Piotr:

    If you mean that there is no such mechanism known to you, I’m prepared to believe you. Perhaps hou’ve never heard of domain duplication, insertion, gene fusion, recruitment of transposable elements, etc.

    Please demonstrate that any of those can add to the AA length of an existing protein. Next tell us how it was determoned those changes are accidental.

    As I said you have no evidence that gene dupication is accidental. As I said that all goes back to the OoL- stay focused, indeed.

    And again there isn’t enough time for chance to do it, Piotr. You are asking way to much of luck, and that ain’t science.

  69. 69
    Evolve says:

    Quote mining.

    The author conveniently left out the following sentences from Carl Zimmer’s article hoping that most readers won’t notice it:

    “One reason it no longer seems so improbable is that Dr. Begun and other researchers have documented the step-by-step process by which a new gene can come into existence.
    In many species, ours included, protein-coding genes make up a tiny portion of the genome. New genes can emerge from the vast expanse of noncoding DNA.
    The first step is for a tiny bit of DNA to mutate into what scientists call a “start sequence.” All protein-coding genes have start sequences, which enable cells to recognize where genes begin.
    Once a cell recognizes the start of a gene, it can make a copy of the gene’s DNA. It can then use that copy as a guide for building a protein.
    The new protein may turn out to be toxic, or it may serve no purpose. But once it emerges, new mutations to the new gene may make it more useful.
    “Once they’re produced, there’s an opportunity for natural selection to sculpt them,” said Aoife McLysaght, a geneticist at Trinity College Dublin.
    Dr. Begun and his colleagues are now getting a look at these early stages in the birth of de novo genes. They can do so by looking for such genes in different populations of a species of the fruit fly Drosophila melanogaster.”

    The author wants to hide the fact that new genes have been shown to arise from ancestral non-coding DNA by the well-understood process of mutation.

  70. 70
    Mung says:

    Joe:

    Mung, Nice quote mine of Spetner. The part you quoted has nothing to do with what I am saying. Spetner also talks about long term changes, Mung.

    Sorry, but that just happened to be where I had left off reading for the night. The following paragraph in the book is just a bunch of handwaving.

    It’s as if y6ou have turned into an evo

    It’s as if I’ve made the same arguments against young earth creationism ever sine I’ve been here. They can’t make up their minds whether they are pro or anti evolution.

    Even you seem to be conflicted. Is God creating new orphan genes, as Jehu thinks, or do they arise as a matter pre-programming through non-random evolution?

    What’s the difference between God the programmer and God the clockmaker who winds things up and then they run on their own?

  71. 71
    Mung says:

    Piotr:

    Have you got a creationist/designist explanation of the fact that orphan genes in humans (similarly to those in other species) don’t encode for complex proteins, that they are all single-copy genes…

    Are these “young orphan genes” and how would you know? Is it because they are short and don’t code for anything all that complex? Because there are no duplicates of them?

    For example, if you could show me a young orphan gene that encodes for a large and highly complex multi-domain protein involved in some really important interactions, I’d agree that the spontaneous rise of such a structure by accident is not a satisfactory explanation.

    If shown such an orphan gene, would you say it could not be young, because young orphan genes just don’t encode for large and highly complex multi-domain proteina involved in really important interactions and must have duplicate copies?

    Why are numerous short functional orphan genes more probable than a single one that codes for a complex protein?

  72. 72
    gpuccio says:

    Piotr and all:

    Let me hijack again a few facts.

    The paper you quoted derives its facts mainly from another important paper:

    “Origin of Primate Orphan Genes: A Comparative Genomics Approach”

    http://mbe.oxfordjournals.org/.....3.full.pdf

    which is very good, and that I invite everybosy here to read, because it is the kind of paper that hijackers like me do prefer: many facts, and mainly honest and interesting empirical interpretations.

    Some examples of honest and interesting interpretations:

    We have determined that primate orphan genes evolve about four times faster than the average gene. Such rapid evolutionary rates may be related to relaxed functional constraints on proteins with newly acquired functions and/or to positive selection linked to adaptive evolution

    Emphasis mine.

    It has recently been argued that most of the annotated human orphan proteins are likely to be spurious ORFs that are not functional (Clamp et al. 2007). Here we only considered human gene products that showed significant similarity to putative macaque and chimpanzee proteins and, with this data set, we reached quite different conclusions regarding the possible functionality of orphan genes.

    And many other good things.

    Is there darwinist propaganda here? Well, just a little bit, at the end:

    These studies have revealed that a much larger fraction of the genome than previously thought is found in primary transcripts, potentially increasing the opportunities for new gene functions to arise. Short ORFs present in such transcripts could occasionally be translated into new peptides, which would then be tested by natural selection. If advantageous, the new function would be retained and continue to evolve. We hope our results will encourage further studies on the evolutionary and functional implications of newly formed genes.

    OK, this is propaganda, but it is expressed with great caution (note the many semantic tags of wishful thinking), and it is at the end, completely separated from the facts in the paper, completely independent from the interesting conclusions in the paper. IOWs, just a due homage to the party line.

    Now, let’s go to the interesting facts, and do a little criminal hijacking.

    A very important part are the results in Table 3 about the 270 primate de novo genes they studied:

    Categories of Primate Orphan Genes:
    Mechanism of Formation
    of Primate Orphan Gene:

    Gene duplication: 66 (24%)
    Exaptation from TEs: 142 (53%)
    De novo formation from noncoding regions: 15 (5.5%)
    Unknown: 47 (17%)

    This is really interesting. De novo formation is an inportant and well documented mechanism (5.5%), as is the traditional model of gene duplication and variation (24%), but the main mechanism, by far, seems to be the one I love most: transposons (53%).

    The important points:

    a) None of these three mechanisms has any potential to generate functional protein information, if unguided. All of them require a design intervention to happen as we observe them, with the functional results we observe.

    b) Transposon variation should be the least related to function, the most devastating. Instead, it is exactly the one which generates most function.

    c) The 270 new genes have documented function in 6 cases:

    – dermcidin, encoding a peptide secreted in sweat glands with antimicrobial activity, which has also been reported to be involved in neural survival and cancer

    – a role in immune response (minor histocompatibility protein HB-1, which is able to stimulate T-cell responses)

    – the SPHAR gene (S-phase response), involved in the regulation of DNA synthesis

    – two more genes, FAM9B and FAM9C, exclusively expressed in testis, have been suggested to play roles in mediating recombination during meiosis

    – one protein from the primate specific morpheus gene family has been shown to locate in the nuclear pore complex

    As you can see, these seem rather noble, refined functions.

    According to the facts presented by the authors, the properties of the other 264 de novo genes are similar to those of the 6 for which a function has been shown. That is a good point for the possible functionality of all or most of them.

  73. 73
    Piotr says:

    None of these three mechanisms has any potential to generate functional protein information, if unguided. All of them require a design intervention to happen as we observe them, with the functional results we observe.

    Define “function” and explain to me why it’s impossible to acquire a function without divine disine design intervention.

    As you can see, these seem rather noble, refined functions.

    They are just “functions” of sorts. I fail to see what’s noble or refined about them.

  74. 74
    gpuccio says:

    Piotr:

    Short comments to my long posts. But it’s better than nothing.

    I have been defining function and functional complexity for years here. I have also defined in detail my specific concept of functional complexity, dFSCI (digital functionally specified complex information). And I have shown many times why dFSCI can be empirically linked to design with 100% specificity, and therefore used as an extremely good tool for design inference. I am preparing an OP on the subject, but I need some more time to finish it.

    I have also debated that on other non design blogs, like TSZ (The Skeptical Zone). There was also a long challenge about dFSCI between me and those at TSZ.

    However, I will try to give you some inputs from recent posts of mine on the subject:

    1) From a debate with Jerad two years ago:

    So, in a nutshell:

    a) Design is the act by which conscious intelligent beings, such as humans, represent some intelligent form and purposefully output that form into some material system. We call the conscious intelligent being “designer”, and the act by which the conscious representation “models” the material system “design”. We call the material system, after the design, a “designed object”.

    b) Some designed objects (not all) have a specific property, objectively verifiable, that we call “CSI”: that is, they bear meaningful information (the design), and that meaningful information is complex.

    c) A specific form of CSI is what I call “dFSCI”, that is CSI that is both digital and functionally specified. Let me confine the discourse to this form, for the moment.

    d) For all the objects we can observe in our reality, and whose origin is known, it can be always verified that any object exhibiting dFSCI has been designed by a conscious intelligent being (in practice, some human). No counterexample exists.

    e) Of all the objects we can observe in our reality, except human artifacts, only one category, whose origin is at least controversial, exhibits dFSCI. That category is biological objects.

    f) It is perfectly reasonable, therefore, to hypothesize that biological objects are designed. That naturally brings to the question of what kind of conscious intelligent agent designed them, but that question in no way makes the inference less valid.

    g) If you and your similar cannot even accept the above inference as a valid scientific hypothesis, and indeed as the best explanation at present for biological information, I can only say that you have a methodological problem, and that you are in principle committed to a specific world view and ideology, probably materialistic reductionism, or scientism (which are more or less the same thing). No problem, anybody is free to believe anything. But I cannot count on your scientific objectivity.

    From the same thread:

    The point is not that humans are the only known source of dFSCI (which is empirically true).

    The point is that we are witnesses of the process of design, especially when we ourselves design something. So, we know intuitively that, in the process of design, a mental representation involving meaning and purpose is the true origin of the oordered output that shapes the final physical system. It can be a cognitive representation, or some artistic intuition, or anything else, but the point is always the same: we have to consciously represent what we want to achieve, and how to achieve it, before using our physical body to shape the physical system that will be the “storage tool” of our representations.

    It’s always that way: Meaning and purpose are always the source of design. We have to have a desire, and to know how to satisfy it.

    So, in the end, the simple truth is: any being who can represent, understand and have intent can be a designer. It is not important that it be a human. As the example of aliens clearly shows.

    So the problem is, are humans the only beings who can represent, understand and have intent? Well, the question is at least open to discussion. A very big discussion, I would say.

    Another common objection is that the designer must have access to some physical tool to design. Indeed, we conceive design in our consciousness, but we design through our bodies.

    Now, I will happily admit that the designer needs to manipulate matter to design biological information. And yet, if we exclude the hypothesis of aliens, I will also admit that the most likely scenario for the biological designer(s) is that he is not a physical being with a body. So, what about that?

    Again, are we really sure that any conscious being must have a physical body? I would only say that we know nothing about the final nature of consciousness. If we want to stay empirical, we can only treat it as an objective reality that we perceive subjectively (in ourselves), or infer (quite reasonably) in other beings.

    So, the point is, if it is true (and it is true!) that consciousness cannot be explained in terms of objective aggregations of matter, we must still describe our reality as a continuos interaction between our consciousness and our physical body. That interaction is absolutely real, even if we have no idea of what our consciousness is. Perception and will are the obvious input and output of that interaction.

    So, there is no doubt that our conscious representations do manipulate the physical reality that is our body. (I will not even consider here the squalid view of reductionists, that cosnciousness is only a byproduct of the physical working of the brain, and that no free will exists, and so on. It is a world view that is not only foolish, but completely unsupported by any serious consideration, either scientific or philosophical).

    So, it is a fact that our conscious representations are influenced and do influence our physical body. How does that happen?

    We don’t know, but here we have something very similar to what the biological designer does with living beings: he influences them starting from his conscious representations. What we daily do with our brains, he can do with biological beings.

    Is that so strange? Not to me. It has never been strange for billions of intelligent human beings who have lived and still live on our planet, and who have intelligently, consciously, seriously believed in the existence of some form of spiritual intelligence that can interact with our world, and does exactly that. I do believe that, like them, like many, and I will not accept that my worldview, that I find simple, beautiful and deeply satisfying both for my intellect and for my heart, should be considered less “scientific” than anyone else’s only because it is different from the shared dogma of our generation.

    OK, maybe I have said too much, but sometimes one just needs to state things as they are.

    You can also look at my OP about design definition, here:

    http://www.uncommondescent.com.....ng-design/

    Or, for more detail look at my posts 680, 682, 684, 685, 686, 687, 688, 689, 691, 693, 694, 695 (and many others following and analyzing TSZ’s objections) here:

    http://www.uncommondescent.com.....ent-434682

    For an example of computation of functional information in protein families, please read the fundamental Durston paper:

    “Measuring the functional sequence complexity of proteins”

    http://www.tbiomed.com/content.....2-4-47.pdf

    If you are interested, I am fully available to discuss any specific aspect of the issue again with you. Whenever you like.

    Finally, my simple idea is that functions related to the neural system, or the immune system, or the reproductive system, are “high level” functions. For example, the de novo genes identified in drosophila were expressed in the testis. The idea is that de novo genes active in the neural system, the immune system and the testis are prominent in recent speciation. There are data suggesting that, IMO, also in the recent FANTOM5 papers. If I have time, I will try to comment on them.

  75. 75
    Piotr says:

    Short comments to my long posts. But it’s better than nothing.

    I wasn’t asking for much. For starters, let’s discuss something very specific. Not “digital functionally specified complex information” linked to intelligent design “with 100% specificity”, but plain old “function” in the sense that biologists attach to this word. Why do you think it requires a miracle (or intervention by supernatural forces) for a protein sequence shorter than 100 amino acids to acquire some sort of function? Mind you — any functionality will do. It doesn’t have to be noble and refined to be promoted by positive selection. You say it’s against all probabilistic odds. How on earth do you know?

    And while we are at it: why are all de novo genes like that? Why (if they encode for a protein) the product is short and its function (if identifiable at all in the first place) is rather marginal? What prevents the designer (who, it would seem, is practically omnipotent in matters of genetic engineering) from creating big complex pepitide chains — hundreds or thousand aa long de novo? I asked Joe this question and he evaded answering it. Perhaps you have a good answer. But please make it concise. I do not like the Gish gallop.

  76. 76
    gpuccio says:

    Piotr:

    a) It is complex functional information which cannot be generated randomly. Simple functions can emerge randomly, but they do not lead to complex functions. Known example of microevolution are 1 -2 AAs (less than nine bits).
    I have proposed a threshold of 150 bits of functional information for design inference in biological objects. Behe and Axe, from observed models, stick to 3 – 5 AAs (which would be less than 22 bits). Many proteins are beyond the 500 bit threshold (Dembski’s UPB), as you can see from Durston’s paper.

    b) What about primate de novo genes? It is true that they are rather short proteins, but not so shoort: The mean length is 100 AAs, with a median og 90 and a SD of 53. That means that many of them are definitely longer than 100 AAs.
    If you read the paper, you will see that oler proteins are longer throughout natural history.
    I have recently pointed to ATP synthase, which is extremely long and complex just from the beginning. Subunit beta shows more than 300 AA identities between E. coli and humans. It is not an old protein which became complex in time. It is an old protein which was complex when it started.
    The reason why more recent proteins become shorter in time is probably another one: they have different types of functions, more regulatory and less basic.

    b) It does requires a design intervention for any protein gene (or any other digital sequence) to acquire more than a definite threshold of complex functional information (let’s say more than 150 bits, 35 fixed AAs, to stay conservative).

    c) Any functionality will do, but to be selected a functionality must confer a reproductive advantage. Let’s say that any naturally selectable functionality will do.
    And, if we know the function and its molecular basis, we can compute the functional complexity for that specific function.
    And simple, stepwise functions, if and when they exist, do not build complex functions, except in the imagination of neo darwinists (can I use the word?).

    d) Why do you say that the function of de novo genes would be “marginal”. On what empirical basis? The functions of the 6 of them which are known are not marginal. Primates are different from other mammals, aren’t they? But they share all basic genes, like ATP synthase, with older species, even with bacteria. Most researchers agree that the difference in higher species is mainly regulatory. Would you call that difference “marginal”?

    e) You ask:

    “What prevents the designer (who, it would seem, is practically omnipotent in matters of genetic engineering) from creating big complex pepitide chains — hundreds or thousand aa long de novo?”

    Nothing. Indeed, he has done that: at OOL, and in the first phases of protein evolution. ATP synthase is a good example. Remember, ATP synthase, like any new basic protein, was a de novo gene when it first appeared.

    I hope I have been concise enough. When I give only a short comment, you accuse me of “rigmarole of lies”, When I try to give you details to answer a specific question which I have been debating for years, you accuse me of Gish gallop.

    I can be as short or as long as you like. It only depends on your questions and your interest.

  77. 77
    Joe says:

    Who cares about proteins with a length shorter than 100AA? Most proteins are much longer than that. And there is no way to get longer proteins once you have one.

    What prevents the designer (who, it would seem, is practically omnipotent in matters of genetic engineering) from creating big complex pepitide chains — hundreds or thousand aa long de novo?

    Nothing and obviously it happened at the OoL- the intervention event. However now there isn’t any intervention now. Organisms have to rely on their built-in responses to environmental cues- most of which occur within the immune system- something else that unguided evolution cannot explain.

  78. 78
    Joe says:

    Evolve:

    The author wants to hide the fact that new genes have been shown to arise from ancestral non-coding DNA by the well-understood process of mutation.

    LoL! Being well understood doesn’t make it unguided. The processes that run my computer are well understood. The processes that run my car are well understood.

  79. 79
    Piotr says:

    What about primate de novo genes? It is true that they are rather short proteins, but not so shoort: The mean length is 100 AAs, with a median og 90 and a SD of 53. That means that many of them are definitely longer than 100 AAs.

    It means that some of them are somewhat longer, but nowhere near the average length of older proteins. Those that are specific to Eukarya, for example, have lengths in the 500-600 aa range (and some may be twice or more as long). And note that you are talking about primate TRGs now. They are in fact quite old (~ 65 million years).

    If you read the paper, you will see that ol[d]er proteins are longer throughout natural history.

    Precisely. Why should that be the case?

    The reason why more recent proteins become shorter in time is probably another one: they have different types of functions, more regulatory and less basic.

    This is completely ad hoc. Let’s try again: what prevented the designer from adding something “more basic” to a genome in recent times?

    You ask:

    “What prevents the designer (who, it would seem, is practically omnipotent in matters of genetic engineering) from creating big complex pepitide chains — hundreds or thousand aa long — de novo?”

    Nothing. Indeed, he has done that: at OOL, and in the first phases of protein evolution. ATP synthase is a good example. Remember, ATP synthase, like any new basic protein, was a de novo gene when it first appeared.

    This is a red herring. My question was not about genes with three-billion-year-old pedigrees (we don’t call them de novo genes) but about recently formed orphan genes. Why can’t their products be anywhere as complex as those of phylogenetically old genes (such as the ATP family)?

  80. 80
    Joe says:

    Piotr- your entire position is completely ad hoc. So perhaps you should just stop and face the music.

  81. 81
    Piotr says:

    @Joe

    Excuse me if I ignore your peanut gallery heckling.

  82. 82
    Joe says:

    Piotr- I don’t care what you do. I am positive that you will never provide any evidence for unguided evolution producing de novo genes. And that is all that counts.

    IOW you are the peanut gallery

  83. 83
    gpuccio says:

    Piotr:

    a) In Durston’s paper, the minimum functional complexity found is 46 bits, for Ankyrin, which is 33 AAs long. All proteins longer than 65 AAs have more than 150 bits of functional information (except one which is 123 bits). Unless de novo genes are completely different from all other functional proteins we know of, their functional complexity cannot be explained by random variation.

    b) Proteins are longer when they are older. But that’s not because they start short and gradually become longer. Older proteins start longer, and more recent proteins start shorter. And remain shorter. As I have shown you with the example of ATP synthase, proteins do not grow in length and complexity with time. I could give many other examples.
    Therefore, the reasonable explanation for shorter proteins in more recent history is that different kinds of proteins and of functions become necessary at different steps of evolution. This is not ad hoc, it is simply what facts suggest. Your theory, that proteins start short and scarcely functional, and are elongated with time, is simply wrong: facts do not support it.

    c) You ask: “Let’s try again: what prevented the designer from adding something “more basic” to a genome in recent times?”
    It seems that either the designer or unguided evolution added proteins which are shorter as time passes and remain shorter. How do you explain that? O have given an explanation. What is yours?

    d) You ask: “My question was not about genes with three-billion-year-old pedigrees (we don’t call them de novo genes) but about recently formed orphan genes. ”

    But the point is that the “shorter” rule is equally valid for old pedigrees. In the paper, you can see that the mean prtein length in vertebrates is 624 AAs, while in mammals it is 329. That is a big difference. How do you explain it? You cannot evade the question just saying that “we dn’t call them de novo genes”. As I have said, each new gene is a de novo gene when it appears.

    So, why are mammal de novo genes less complex that vertebrate genes?

  84. 84
    jerry says:

    A large percentage of these questions about de novo genes will be answered in the next 15-20 years as more genomes get sequenced. Something does not come from nothing without leaving a trail in the genomes of related species. If the trail is there then most if not all the history of a gene will be available. If it is not there, then that will be a major mystery for those who propose naturalistic evolution.

    What may be of interest now is just how many genes have a known history as to how they developed. I am not talking about speculation or just told stories but genomic forensic evidence. Which one of the 50 engines of variation did each gene begin with, how did it change over time, why did some populations get the functional sequence while others did not. Does any of it challenge Axe and Durston’s ideas? So far I haven’t seen too many explanations but they should come if they exist.

    What will probably dominate biology is not de novo genes but the origin of the control mechanism in the genome. Control mechanisms in the human genome are apparently incredibly more complex than its nearest so called cousin, the chimp. How did these networks arise? Must have happened somewhere in Africa because all were established when humans left Africa. And why didn’t this process spawn many other species with equal or slightly less complex control mechanisms. A mystery!

  85. 85
    gpuccio says:

    Piotr:

    Another example on which you could reflect.

    RAG1 is an important protein which effects DNA recombimnation in the adaptive immune system. The adaptive immune system is foung only in vertebrates, and it originated in jawed fish approximately 500 million years ago. That’s when the RAG1 protein appears.

    Now, i did a simple blast of the protein in zebrafish and the protein in humans.

    The result:

    Protein length:

    Zebrafish: 1057 AAs
    Human: 1043 AAs

    Score
    1249 bits(3231)

    Expect 0.0

    Identities: 632/1067(59%)

    Positives: 786/1067(73%)

    The final two thirds of the two molecules are practically identical.

    Now, if this important protein appeared in jawed fish, and if it retains practically the same length and sequence in humans, it is obvious that it had more or less the same length and sequence when it appeared in the first jawed fish. IOWs, when it was a de novo gene.

    How do you explain that?

  86. 86
    gpuccio says:

    jerry:

    So far I haven’t seen too many explanations but they should come if they exist.

    An easy prediction. You will not see them, because they don’t exist.

  87. 87
    Piotr says:

    In Durston’s paper, the minimum functional complexity found is 46 bits, for Ankyrin, which is 33 AAs long. All proteins longer than 65 AAs have more than 150 bits of functional information (except one which is 123 bits). Unless de novo genes are completely different from all other functional proteins we know of, their functional complexity cannot be explained by random variation.

    I suppose you mean Durston’s “fits”, units related to, but not identical with ordinary “bits”. Is there a magic threshold above which complexity is not evolvable? If so, what is it and how do you know?

    Proteins are longer when they are older. But that’s not because they start short and gradually become longer. Older proteins start longer, and more recent proteins start shorter. And remain shorter.

    OK, I’ll repeat ad nauseam if necessary: why should it be the case?

    As I have shown you with the example of ATP synthase, proteins do not grow in length and complexity with time. I could give many other examples.

    If they are very important and highly conserved, stabilising selection conserves their size as well. It doesn’t mean that the ATP gene family sprang into existence ready-made.

    I do not claim that all proteins evolve by consistently increasing their length and complexity — only that they begin their evolutionary career as relatively short and unsophisticated structures.

    Your theory, that proteins start short and scarcely functional, and are elongated with time, is simply wrong: facts do not support it.

    First, it isn’t my theory; it reflects the consensus of those who know more about protein evolution than either of us. Secondly, it is consistent with the statistics relating the mean length of proteins to their evolutionary age.

    If you don’t mind, I would appreciate some information about the flavour of ID that you prefer. Guided evolution, which accepts universal common decent, speciation, etc., over billions of years, but “the designer” is required to tweak the genome every time when some new function is to evolve?

    It seems that either the designer or unguided evolution added proteins which are shorter as time passes and remain shorter. How do you explain that? O have given an explanation. What is yours?

    Your answer is a non-explanation. We still don’t know why “the designer” behaves in this fashion. My explanation is simple: I reject your assertion that protein length can’t evolve.

    So, why are mammal de novo genes less complex that vertebrate genes?

    The first vertebrates are more than twice as old as the first mammals. When the mammalian de novo genes arose, the vertebrate ones had already been evolving for 300 million years.

  88. 88
    Piotr says:

    Now, if this important protein appeared in jawed fish, and if it retains practically the same length and sequence in humans, it is obvious that it had more or less the same length and sequence when it appeared in the first jawed fish. IOWs, when it was a de novo gene.

    How do you explain that?

    How do you know what it looked like when it started evolving de novo? The protein was apparently complex and well conserved already in the last common ancestor of humans and zebra fish. But was the gene encoding for it a true de novo one at the time? It seems to have homologues among the Transib transposons, and its core sequence has been found in other deuterostomes (amphioxi and echinoderms). See https://en.wikipedia.org/wiki/Recombination-activating_gene#Evolution

  89. 89
    Mung says:

    Joe:

    Nothing and obviously it happened at the OoL- the intervention event. However now there isn’t any intervention now. Organisms have to rely on their built-in responses to environmental cues- most of which occur within the immune system- something else that unguided evolution cannot explain.

    A fine statement of young earth creationism. God started it all off then it was hands off, everything else mechanistic.

    Evolution.

    Can we call this intelligent PRE-DESIGN so as to distinguish it from intelligent design?

    Does part of that pre-design preclude species from eventually evolving into new “kinds”?

  90. 90
    Piotr says:

    Jerry:

    Control mechanisms in the human genome are apparently incredibly more complex than its nearest so called cousin, the chimp.

    Have you got a reference for that? It’s widely believed that the differences between humans and chimps are mostly due to differences in gene regulation, but it doesn’t follow that the regulatory networks of the human genome are “incredibly more complex”. They are just different for some key genes.

  91. 91
    Mung says:

    Piotr:

    I do not claim that all proteins evolve by consistently increasing their length and complexity — only that they begin their evolutionary career as relatively short and unsophisticated structures.

    That’s right. And we’re not saying you contradict yourself, for you are obviously arguing that not all proteins are long and sophisticated. Especially not the young ones.

    But it’s a reasonable inference on our part, is it not, that you do believe that older proteins started out just like younger ones, as relatively short and unsophisticated? Relative to what?

    The older and relatively longer and more sophisticated proteins did not just pop forth that way de novo, did they?

    And that’s the question gpuccio is asking you. What’s your evidence for the gradual increase in length over time and increased specificity over time and heightened complexity over time of the older proteins?

    How are you not arguing in a circle? See my post @ 71.

  92. 92
    Joe says:

    My explanation is simple: I reject your assertion that protein length can’t evolve.

    And when you have some evidence to support your “explanation”, someone will listen.

  93. 93
    Joe says:

    Doug Axe, in an eaasy in “The Nature of Nature”, explains why protein length doesn’t grow. I’ll have another read of it later

  94. 94
    Joe says:


    Nothing and obviously it happened at the OoL- the intervention event. However now there isn’t any intervention now. Organisms have to rely on their built-in responses to environmental cues- most of which occur within the immune system- something else that unguided evolution cannot explain.

    A fine statement of young earth creationism. God started it all off then it was hands off, everything else mechanistic.

    That has nothing to do with YEC.

    Evolution.

    ID is not anti-evolution.

    Can we call this intelligent PRE-DESIGN so as to distinguish it from intelligent design?

    If you can show there is a difference. Good luck with that.

    Does part of that pre-design preclude species from eventually evolving into new “kinds”?

    Only if such a thing is possible.

  95. 95
    Piotr says:

    @Mung: OK, back to your post #71

    Are these “young orphan genes” and how would you know? Is it because they are short and don’t code for anything all that complex? Because there are no duplicates of them?

    One of the important criteria for the identification of true orphan genes is the presence of a related non-coding sequence in close outgroups: link

    Why are numerous short functional orphan genes more probable than a single one that codes for a complex protein?

    I’m not sure what you mean by “probable” here. Both simple and complex proteins exist, so there must be possible pathways leading to both.

    I would say that the accidental origin “from scratch” of a gene encoding for a complex functional protein is practically impossible, while the accidental emergence of functionality in a small protein with a random amino acid sequence is possible despite its small probability (see Szostak’s experiments with ATP-binding short proteins randomly generated in vitro).

  96. 96
    Piotr says:

    Mung:

    What’s your evidence for the gradual increase in length over time and increased specificity over time and heightened complexity over time of the older proteins?

    There’s enough evidence of things like exon/domain duplication via unequal crossing-over, for example. You can easily google up any number of examples. Complex proteins are modular, and they can evolve by multiplying and/or shuffling their modules. Again, actual gene families can be used to illustrate it.

  97. 97
    Joe says:

    Reality refutes Piotr:

    In essence, it appears to be physically implausible for the large protein structures we see in biology to have been built up from tiny ancestral structures in a way that: 1) employed only simple mutation events, and 2) progressed from one well-formed structure to another. Simply put, the reason for this is that folded protein structures consist of discrete multi-residue units in hierarchal arrangements that cannot be built through continuous accretion. The material on the outer surface of an accretive structure, such as a stalagmite, is converted to interior material as successive layers are added. For structures of that kind the distinction between exterior and interior is one of time-dependent geometry rather than of substance. By contrast, the process by which proteins fold involves a substantive distinction between interior and exterior that is evident in the final folded form. Since an evolutionary progression from tiny protein structures to large globular ones would have to repeatedly convert exterior surface to interior interface, this means that any such progression would have to coordinate the addition of appropriate new residues with the simultaneous conversion of existing ones. Considering that these structural additions and conversions would both involve many residues, it seems inescapable that one or the other of the above two conditions would be violated. Furthermore, on top of these conditions is the primary consideration in this section- that of function.

    IOW the only way they could have evolved is by design.

  98. 98
    Joe says:

    Quote was from Doug Axe page 420 “The Nature of Nature”

  99. 99
    gpuccio says:

    Piotr:

    I suppose you mean Durston’s “fits”, units related to, but not identical with ordinary “bits”. Is there a magic threshold above which complexity is not evolvable? If so, what is it and how do you know?

    Yes. As I have said, I have proposed 150 bits as a higher threshold for biological evolution of function on our planet by pure random variation.

    Here is a recnt discussion I had with VJ (if you don’t accuse me of “Gish gallop”):

    Let’s talk a minute of the edge of evolution. IOWs, about how much functional variation RV + NS can really do in the real world.

    Behe has put it above two AAs, in his very good book, and considering very good arguments from observable scenarios. Axe, with different experimental consideration, puts it at about 5 AAs. I believe that is probably very true.

    Dembski, with very general considerations, proposes 500 bits (about 116 AAs) as universal probability bound. I have proposed 150 bits (about 35 AAs) starting from a model like the one I posted here.

    You mention 1:10^70 as the number of folding proteins, from Axe again, I believe. That is probably true. But remember, folding is not all. A protein must not only fold to be visible to NS. It must confer a reproductive advantage in a definite environment.

    I often quote the following paper:

    “Experimental Rugged Fitness Landscape in Protein Sequence Space”

    http://www.plosone.org/article…..ne.0000096

    which experiments with a mutated protein in a phage, trying to find the original wild type sequence which confers full infectivity. Well, here RV and NS are acting at their most, starting from a random library of peptide sequences, in a very favorable context (the function is maintained, even if at low levels, so NS can act just from the beginning).

    I always quote the final conclusion of the authors:

    “The question remains regarding how large a population is required to reach the fitness of the wild-type phage. The relative fitness of the wild-type phage, or rather the native D2 domain, is almost equivalent to the global peak of the fitness landscape. By extrapolation, we estimated that adaptive walking requires a library size of 10^70 with 35 substitutions to reach comparable fitness.”

    Well, 10^70 is the order of magnitude proposed by Axe for folding proteins, and 35 AAs is my “universal biological bound”.

    Coincidences? Probably, but what it means is that we are on the right way, and that our intuitions about the functional space of proteins are quite right.

    Durston has computed functional information for 35 different protein families. Only six of them have functional complexity below 150 bits (my biological bound). All of them are very short peptides (33 -55 AAs). Insulin (65 AAs) already has a functional complexity of 156 bits.

    The biggest protein in the list, Paramyx RNA Pol, has a functional complexity of 1886 bits.

    In my simple model, even if only one new unrelated protein of the median functional complexity of 357 bits, were to be found to confer some definite advantage to a new species, the probability of that single event in 4 billion years, in the whole planet, would still be 5.78e-132.

    IOWs, not a single new protein superfamily of median complexity could ever be generated on our planet by neutral mutations alone. And no functional precursors to superfamilies have ever been shown to exist, so the role of NS in that scenario is nil.

    More in next post.

  100. 100
    gpuccio says:

    Piotr:

    This is another post of mine:

    Thank you for your thoughtful post. We really need more people with biological experience here!

    I think that, when we try to “explain” the evolution of functional sequences, like proteins, the mutation rate can be safely approximated in favour of the darwinian theory: the theory will however fail, and without any possible doubt.

    I will try to be more clear. What really counts here is not the mutation rate itself, but the number of states, or sequence configurations, that can be really achieved by the system in the available time.

    When Dembski proposed his famous universal probability bound, he set the threshold very high (500 bits of complexity, about 10^150 possible configurations), so that he could exclude any possible random search in the whole universe, even using all quantic states from the big bang on as bits for the computation.

    That is really remarkable, because 500 bits is equivalent to the complexity of a 115 AAs sequence (if the target space were made of one single state). Even considering the functional redundancy, we are well beyond that threshold in many complex proteins. For example, in Durston’s famous paper where he analyzes 35 protein families, 12 protein families have functional complexities beyond this universal probability bound, with the highest functional complexity being 2416 bits (Flu PB2).

    But I always felt that Dembski was being too generous here. So some time ago I tried to compute a gross threshold which was more appropriate for a biological system. So, I considered our planet, with a life span of 5 billion years, as though it had been fully covered by prokaryotes from the beginning of its existence to now, and I tried to compute, grossly, the total number of states which could have been tested by such a system, considering a mean bacterial genome, reproduction time, and a very generous estimation of a global bacterial population on our planet. The result, which can be more or less appropriate, was that 150 bits (10^45) of functional complexity were more than enough to exclude a random generation of a functional sequence in the whole life of our planet.

    Now, that is even more remarkable, because 150 bits is equivalent to about 35 AAs, and in Durston’s paper 29 protein families out of 35 were well beyond that threshold.

    Are we still exaggerating in favour of darwinism? Yes, we certainly are.

    First of all, prokaryotic life did not certainly begin 5 billion years ago (which is even more than earth’s real life span).

    Second, the earth was not certainly fully covered by prokaryotes from the beginning of life.

    Third, the appearance of new protein families is not restricted to prokaryotes, but it goes on in higher beings, up to mammals. And mammals reproduce much more slowly than prokaryotes, and, even more important, they are not as many of them on our planet. Therefore, the number of states that can be reached / tested by mammals, or more in general by metazoa, is much smaller than what can be reached / tested by prokaryotes, whatever the mutation rate. And still, new complex functional protein families which never existed before, and are totally unrelated to what existed before, continued to emerge in metazoa, up to mammals.

    So, maybe 150 bits is still too generous as a biological probability bound. After all, both Behe and Axe, starting from bottom up considerations, tend to fix the threshold of what random variation can achieve at 3-5 AAs (about 13-22 bits).

    But I fell that I can safely be generous. We win anyway.

    So, let it be 150 bits, for now 🙂

    More in next post.

  101. 101
    jerry says:

    Have you got a reference for that? It’s widely believed that the differences between humans and chimps are mostly due to differences in gene regulation, but it doesn’t follow that the regulatory networks of the human genome are “incredibly more complex”. They are just different for some key genes.

    Go to

    http://www.uncommondescent.com.....ent-496683

    Here is part of the summary:

    What shall we say about the genes which make us human? We and chimps share 96% to 99% of our protein coding sequences. Why are we different? Not the 1.5% of our genome that codes for proteins but the 98.5% that controls their production. Literally, no other primate lineage has evolved as fast as our lineage has during the last 1.5 million years, and it’s all due to unique changes in our control genome.

    At least 80% probably more of our “non-coding” genome is also transcribed, starting from multiple start points, transcribed in both directions, with overlapping reading frames of many sizes and a whole spectrum of alterations, producing a whole zoo of ‘new’ types of RNA control elements – piRNA,siRNA, miRNA,sdRNA, xiRNA, moRNA, snoRNA, MYS-RNA, crasiRNA, TEL-sRNA, PARs, and lncRNA.

    Most of these unique RNA transcripts – and there are thousands, if not millions of them – are uniquely active in developing human neural tissue – uniquely active compared to their activity in chimpanzees, much less other primates or mammals. It is the new epigenetic world

    Here is the link to the review paper

    http://www.asa3.org/ASA/meetin.....Wilcox.pdf

  102. 102
    gpuccio says:

    Piotr:

    Here I post again the computation for my biological probability bound of 150 bits:

    Just follow me a little bit.

    a) “Simultaneous” obviously does not mean “in one attempt”. What we have to consider is the whole system, which is made of:

    a1) a population size (a number of replicators)

    a2) a mean replication time

    a3) a time span (the time available for the new “species”, or whatever, to appear), IOWs for the transition from A (the precursor) to B (the new thing)

    a4) a mutation rate

    a5) the number of new proteins that characterizes the new state (B) versus A

    a6) the probability for each new protein to arise in a random system, in one attempt

    b) Given those numbers, we can make a few easy computations

    c) I will assume an extremely generous model.

    c1) Out population is the whole prokaryotic population on our planet. I will estimate it at 5*10^30 individuals (I have found that on the internet)

    c2) I assume a mean replication time of one division every 30 minutes

    c3) I assume a time span of 4 billion years (2.1*10^15 minutes)

    c4) I assume a mutation rate of 0.003 mutations per genome per generation (from internet, again)

    c5) I assume that B is characterized, versus A, by 3 new proteins, completely unrelated at sequence level with all the proteins in A, and unrelated one with the others

    c6) I assume the same functional complexity for each of the 3 proteins, of 357 bits (Fits), which is the median value for the 35 protein families evaluated in Durston’s paper.

    Multiplying c1 by c2 by c3 by c4, we get the total number of possible mutations in our system in the time span of 4 billion years. The result, with those numbers, is 1.0512*10^42. That is a higher threshold for the total number of individual new states that can be reached in our system in the time span (if each mutation gives a new state).

  103. 103
    gpuccio says:

    Piotr:

    OK, I’ll repeat ad nauseam if necessary: why should it be the case?

    Proteins are as long as it is necessary for their function. We have seen that the mean length in vertebrates is 624 AAs, but RAG1 is more than 1000. There are short old proteins, and long recent proteins.

    In average, the length becomes lower with time. As I have said, the only reasonable explanation for that is that the kind of function which is necessary in more recent speciation is different, more regulatory and less focused on fundamental biochemical activities.

    Your theory that proteins become longer after starting short has no empirical support. I have made specific examples. You give us some, something real.

    If they are very important and highly conserved, stabilising selection conserves their size as well. It doesn’t mean that the ATP gene family sprang into existence ready-made.

    So, what is your idea? How did the beta subunit of ATP synthase, with its 330 conserved AAS, “spring into existence”? A proteins which is in all living cells?

    And how did the RAG1 protein, with its 700 conserved aminoacids, “spring into existence”? A protein which appears in jawed fish and is ultraconserved up to humans, and has no detectable homolog at all in lamprey, a jawless fish?

  104. 104
    gpuccio says:

    Piotr:

    First, it isn’t my theory; it reflects the consensus of those who know more about protein evolution than either of us. Secondly, it is consistent with the statistics relating the mean length of proteins to their evolutionary age.

    First, as already said I don’t accept ideas out of authority, from anyone. If you report a theory, be ready to defend it yourself.

    Second, the theory needs not only to be “consistent” with protein lengths, a facts that can be better explained in many other ways. It needs to be supported by some observation in the proteome, for example some real cases of proteins which start short and become longer across speciation, while maintaining or improving their function.
    I am waiting.

  105. 105
    gpuccio says:

    Piotr:

    If you don’t mind, I would appreciate some information about the flavour of ID that you prefer. Guided evolution, which accepts universal common decent, speciation, etc., over billions of years, but “the designer” is required to tweak the genome every time when some new function is to evolve?

    Yes. I have always defended that position. To be precise, every time when some new complex function is to evolve, Remember, complex functional specification is the tool to infer design.

  106. 106
    gpuccio says:

    Errata corrige:

    Piotr:

    If you don’t mind, I would appreciate some information about the flavour of ID that you prefer. Guided evolution, which accepts universal common decent, speciation, etc., over billions of years, but “the designer” is required to tweak the genome every time when some new function is to evolve?

    Yes. I have always defended that position. To be precise, every time when some new complex function is to evolve, Remember, complex functional specification is the tool to infer design.

  107. 107
    Piotr says:

    @Jerry

    I asked for a serious reference. This ASA talk is hardly a serious review paper.

  108. 108
    gpuccio says:

    Piotr:

    Your answer is a non-explanation. We still don’t know why “the designer” behaves in this fashion. My explanation is simple: I reject your assertion that protein length can’t evolve.

    It’s not my assertion. It’s only that we don’t observe anything like that. Again, give empirical support to that idea.

    The first vertebrates are more than twice as old as the first mammals. When the mammalian de novo genes arose, the vertebrate ones had already been evolving for 300 million years.

    So, RAG1 is 1040 AAs long because it started short at the beginning of the vertebrate radiation? But then how is it that 632 AAs are absolutely conserved up to humans, and 786 are similar?

    Facts please, not imagination. I have given you some definite facts.

  109. 109
    Piotr says:

    @gpuccio, #102

    I don’t see where in your model allowance is made for things like internal duplication. Of course if you only consider point mutations, you argue against a straw man.

  110. 110
    Piotr says:

    So, RAG1 is 1040 AAs long because it started short at the beginning of the vertebrate radiation?

    I never said that. I pointed out that there’s strong eveidence against its gene being a de novo one in early vertebrates.

  111. 111
    gpuccio says:

    Piotr:

    I don’t follow you. What would be the role of duplication to explain the things I have outlined? Please. explain.

    I can make allowance for any kind of random variation. Nothing changes. I used the term mutation to mean any possible random variation. What counts is the number of states which can be randomly reached in the system, in the time span. Each variation is a new state.

    So no, I am not arguing against a straw man. I like to argue against men in flesh and bones.

  112. 112
    gpuccio says:

    Piotr:

    I never said that. I pointed out that there’s strong eveidence against its gene being a de novo one in early vertebrates.

    What “strong evidence”? It appeared in vertebrates as a de novo gene(I know, there is some isolated homology in a couple of isolated species, which is really difficult to explain, whatever the theory one supports: are you referring to that?)

    The fact remains that jawless fish, and practically all other species except vertebrates, have no trace of it.

  113. 113
    jerry says:

    I asked for a serious reference. This ASA talk is hardly a serious review paper.

    You obviously did not read it. It is about as serious as it gets. There are hundreds of references backing up every thing Wilcox says.

  114. 114
    gpuccio says:

    Piotr:

    OK, here is the blast of RAG1 in zebrafish agianst its homolog in Strongylocentrotus purpuratus (a sea urchin):

    Length:

    Zebrafish 1057

    SP 983

    Identities: 244/1010(24%)

    Positives: 402/1010(39%)

    Expect:. 1e-55

    I agree that it is a strong homology, but completely isolated. However, we have here 244 identities. In humans, we have 632. 632 – 244 = 388.

    And the length of the SP is almost the same (983 AAs).

    So, even if the protein in SP is a precursor (but then , why was it lost in all other species preceding vertebrates), still 388 fixed AAs are to be explained after that precursor.

    I must admit that this strange observation would be a good argument against CD!

  115. 115
    Piotr says:

    gpuccio:

    The fact remains that jawless fish, and practically all other species except vertebrates, have no trace of it.

    You mean gnathostomes (lampreys are also vertebrates). But homologues have been found in outgroups (lancelets, starfish and sea urchins), which militates against its de novo origin in gnathostomes and suggests the loss of the gene in lampreys and hagfish as an alternative. Note that even when studying “modern” orphan genes researchers cautiously check a number of criteria before they declare a gene an orphan, ruling out all other explanations. By contrast, you recklessly laim such a status for a gene that must be 500+ million years old. It’s a cavalier approach.

  116. 116
    gpuccio says:

    Piotr:

    The second “exception”, Branchiostoma floridae, is much less stunning. There is only a partial alignment of interest. Here is the blast:

    Length:

    Zebrafish 1057

    BF 1204

    Identities: 29/90(32%)

    Positives 48/90(53%)

    Expected: 3e-06

    Nothing really important here.

  117. 117
    gpuccio says:

    Piotr:

    As you can see, I have already answered.

    The problem is that new protein superfamilies appear all the time without any detectable homologue which can explain their random evolution, least of all naturally selectable intermediates.

    The problem here is not to argue about how to use the term “orphan” or de novo, but to explain how and why new complex sequence information arises against all probabilistic considerations. I think you are trying to evade the real issue. Your choice.

  118. 118
    Piotr says:

    What would be the role of duplication to explain the things I have outlined?

    I mean internal duplication, e.g. when a whole exon is duplicated. It isn’t something that could be achieved by point mutations accumulating over a zillion years.

  119. 119
    Piotr says:

    @gpuccio

    It’s past midnight where I am. I shall be back tomorrow if I find the time.

  120. 120
    gpuccio says:

    Piotr:

    It’s past midnight where I am too. See you tomorrow, if possible. 🙂

  121. 121
    Joe says:

    Piotr’s premise is nothing but wishful thinking. And why does similarity automatically mean homologs? Talk about weak thinking.

  122. 122
    Mung says:

    Hi Piotr,

    Thank you for your response and your posts. I have really enjoyed reading the posts in this thread. This is good stuff!

    I see you’re getting it from all sides, so I will will try not to expect you too respond to every single point. 🙂

    I’ll try to summarize what I see as some of the issues.

    How do we know how young or how old an orphan gene is? It’s not like we’re looking at DNA from long dead organisms! (except by inference)

    If it’s relatively short and only somewhat complex, then it’s young, just doesn’t seem satisfying.

    Regarding probabilities, you seem to think it more likely that there will be many young simple orphan genes than that there will be one or a few old complex orphan genes. But what makes one more probably than the other?

    It’s as if you’re saying simple function is easy to find but complex function is not, so we are more likely to find instances of simple function than instances of complex function. But this is based on what?

    Again, please don’t feel you have to respond to all points.

    Complex proteins are modular, and they can evolve by multiplying and/or shuffling their modules. Again, actual gene families can be used to illustrate it.

    I still have a great deal to learn in this area, so what do you mean by modular?

    Are you talking about modular protein domains? Are you saying that all complex proteins are modular, and if so in what sense?

    Protein domains represent the minimum levels of organization that provide a stable globular core…modular domains tend to be stable and fold on their own…they are not only folding modules but functional modules.

    …Most protein adaptor domains are relatively small, comprising 60 to 130 amino acids. This is sufficient for a shallow concave binding site that can interact with a flexible peptide, carbohydrate, or lipid. These binding sites differ from most enzyme active sites, which usually lie between two domains and are able to take two or more molecules out of the aqueous environment. The nature of the binding site of adaptor modules has a number of interesting consequences for the functions of protein modules…The small size of the core binding region also means that there is often insufficient interaction to allow specificity.

    Modular Protein Domains

  123. 123
    gpuccio says:

    Piotr:

    To sum up:

    a) I believe that the lower length of new genes in more recent species can be interpreted according to different functional requirements, essentially regulatory.

    b) You suggest that it is evidence that they are young and therefore scarcely functional, and that function evolves with protein length in time.

    I say that there is no evidence of this strange theory. Protein families have long or short sequences according to different functional requirement, not according to how old they are.

    IOWs, length variation is maximal between families, and is minimal inside one family.

    To show my point, I have collected some data about 6 different important and old proteins, proteins which appeared “at the beginning”, and which are still there, in humans. I have taken 3 aminoacyl tRNA synthetases and 3 glycolisis enzymes.

    Here are the data:

    The proteins:

    1) Glutamate–tRNA ligase
    2) Valine–tRNA ligase
    3) Alanine–tRNA ligase
    4) Pyruvate kinase
    5) Triose phosphate isomerase
    6) Phosphoglycerate mutase

    The data:

    E. coli Id C. El Id Human Elong.
    1) 471 31% 481 38% 523 11,04%
    2) 951 40% 1050 54% 1264 32,91%
    3) 876 39% 968 58% 968 10,50%
    4) 470 46% 558 58% 574 22,13%
    5) 254 48% 247 62% 286 12,60%
    6) 413 50% 434 75% 434 5,08%

    There is the length in E. coli, in C. elegans and in humans, and the % identity with the human proteins. Finally, there is the percent elongation of each protein from coli to human, which, as you can see, is present but small (from 5% to 32.9%). Instead, the variation in length between different proteins in coli is much large, from 254 to 951, a 274% difference.

    Which is exactly my point.

    I believe that the small increase in length inside a family can be easily explained in terms of adaptation to different, and more complex, cellular contexts, while there is no reason to believe that it is related to an increase in the basic function, which, as far as we know, is efficiently performed by all these proteins, each one in its cellular context.

  124. 124
    gpuccio says:

    Piotr:

    Another important aspect. Please, look at the following recent paper:

    “Emergence of novel domains in proteins”

    http://www.biomedcentral.com/c.....-13-47.pdf

    The point is: new domains have the same length as old domains (about 150 AAs is the mean, and indeed mammalian domains are a little beat longer than old ones), while old proteins are often longer than younger ones, and the simple reason is that they have higher domain numbers (see Table 1 and Table 3).

  125. 125
    Piotr says:

    @gpuccio:

    You suggest that it is evidence that they are young and therefore scarcely functional, and that function evolves with protein length in time.

    I say that there is no evidence of this strange theory. Protein families have long or short sequences according to different functional requirement, not according to how old they are.

    That’s why I asked you if you accepted evolution (even assuming that it was intelligently guided) and the phylogenetic time depths established by mainstream science. If so, you should somehow account for the fact that the mean length of taxon-restricted proteins (which might plausibly have a de novo origin near the root of the taxon) increases with their age.

    I’ll soon return to the question whether proteins may get longer and more complex in the course of time without intelligent guidance, responding both to you and Mung. I have to say I’m enjoying this discussion. It’s quite stimulating. A small DISCLAIMER is perhaps in order: — I’m a linguist, not a biologist, so don’t expect me to be a spokesman for professionally practised evolutionary biology. I’m taking part in this discussion at my peril, out of my personal curiosity, and represent only myself. Any errors or knowledge gaps are entirely my own.

  126. 126
    gpuccio says:

    Piotr:

    I’m taking part in this discussion at my peril, out of my personal curiosity, and represent only myself. Any errors or knowledge gaps are entirely my own.

    That’s absolutely true of me too (by the way, I am a medical doctor). That’s how I like it.

    And I am enjoying the discussion too! As I said in the beginning, you are a very good adversary.

  127. 127
    Joe says:

    Piotr:

    I’ll soon return to the question whether proteins may get longer and more complex in the course of time without intelligent guidance

    Hopefully you have some actual evidence. The say-so of a linguist is meaningless.

  128. 128
    Joe says:

    Piotr’s problems:

    If you have a small and functional protein, that means it has a substrate, the portion of the protein that catalyzes a reaction. If you add on to that protein you are going to bury that substrate which means it may not be accessible depending on whether any properly charged channels were left open to said substrate. Yes the channels have to be properly charged or else the materials required will not make it to the substrate.

    Then you need properly charged channels for exiting the protein once the reaction is finished.

    Doug Axe goes over this in his essay in “The Nature of Nature” see catalase (for example)

  129. 129
    gpuccio says:

    Piotr:

    Some other aspects I would like to clarify.

    I am more than ready to account for the fact that “the mean length of taxon-restricted proteins (which might plausibly have a de novo origin near the root of the taxon) increases with their age”. Facts must always be taken into consideration.

    And I have offered my reasonable explanation: of the length of taxon restricted genes constantly increases with their age, it is probably because the functional requirements for new proteins are different as evolution goes on. At OOL and in the first stages, a lot of new superfamilies had to be designed in a relatively short time, and they had to cover a lot of basic biochemical “miracles”, without which life could not exists. As time goes by, and design focuses more on the expression of new functions, built on the basic functions that already exist, the type of protein required slowly changes. In the last phases, new proteins are mainly requested for specific, high level regulations, while most of the functional novelty comes from modifications, still only partially understood, in non coding DNA or other regulatory structures (epigenetic).

    This is, IMO, a very reasonable scenario. It explains not only the lower length of new taxon restricted genes, but also the slowing rate of appearance of new superfamilies, and the highest modular multidomain structure of ancient proteins.

    I want to specify, too, that the variations we see in proteins through time, and which are so emphasized by neo darwinism, are essentially of one kind:

    Once a new protein superfamily or family, with a defined new structure and function, appears for the first time, it is already unrelated at sequence level with what already exists (that’s implicit in the definition of superfamily: no detectable homologies with the others).

    Then, as time goes by, and new species appear, what happnes is: the protein essentially maintains its strucure and function (with possible tweakings), but the sequence diverges.

    The typical case is similar to proteins like Glutamate–tRNA ligase and Alanine-tRNA ligase, which show still a strong homology between the bacterial form and the human form, usually 30-40% of identities and 50-60% of similarities. Anyway, the sequence is different for a good part, about half of it, but the function is exactly the same: they couple the right aminoacid to the right tRNA. If they did not work correctly in all species, no translation could take place, and life could not exists.

    Just to give an idea, between human and mouse those two proteins have 85% and 96% identity. And still they do the same thing.

    That’s exactly why I believe in common descent.

    What is the reason for that? The best explanation is: The proteins, after they appear for the first time with their functionality, “traverse” their functional space in the course of evolution, because of neutral variation which modifies the function, but do not abandon it, because of negative selection which eliminates most non functional forms.

    That is what is usually called “the big bang theory of protein evolution”.

    Big bang: a new protein appears the first time, with a functional sequence, and then neutral evolution expands the space of sequence, without modifying structure and function.

    That’s what we see in the whole proteome: isolated superfamilies, and then great divergence in the context of the same superfamily or family.

    Of course, there are many cases of tweaking of the function in a family, sometimes with the appearance of a new function, but related to the old structure and function. Nylonase is a good example. Many of those cases are not very complex, implying only a few aminoacids’variation at the active site.

    And of course, there are proteins which are much more conserved between their first appearance and humans, like ATP synthase subunit beta, or RAG1, with their 72% and 59% identities, showing greater than usual functional constraint of the sequence, and resistance to neutral variation.

  130. 130
    gpuccio says:

    Piotr:

    Just a comment on this statement of yours to Mung:

    I would say that the accidental origin “from scratch” of a gene encoding for a complex functional protein is practically impossible, while the accidental emergence of functionality in a small protein with a random amino acid sequence is possible despite its small probability (see Szostak’s experiments with ATP-binding short proteins randomly generated in vitro).

    Without entering in detail here (I have already said too much) I must at least mention that I have criticized extensively that specific paper here, in the past. Szostak has clearly used intelligent selection in the procedure, and his conclusions are not applicable at all to random sequences.

  131. 131
    Piotr says:

    And I have offered my reasonable explanation: of the length of taxon restricted genes constantly increases with their age, it is probably because the functional requirements for new proteins are different as evolution goes on.

    Do you mean that evolution is about to end soon, as new proteins get shorter and shorter? 😉

    That’s exactly why I believe in common descent.

    Good! There is enough common ground to make discussion possible.

    Of course, there are many cases of tweaking of the function in a family, sometimes with the appearance of a new function, but related to the old structure and function. Nylonase is a good example. Many of those cases are not very complex, implying only a few aminoacids’variation at the active site.

    So you are prepared to accept that at least minor functional innovations can occur “by themselves” and do not require the supernatural designer’s personal intervention. Is that right?

    [I’m sorry if I don’t reply at length yet. I’m a little busy today and can’t spend the day glued to the keyboard, but I’ll be back soon.]

  132. 132
    gpuccio says:

    Joe:

    I say this with the greatest respect for you: I agree with you in many things, but why criticize Piotr because he is a linguist? Let’s judge what he says. Authority has no special role here, IMO, while good arguments are good, whoever expresses them.

  133. 133
    gpuccio says:

    Piotr:

    So you are prepared to accept that at least minor functional innovations can occur “by themselves” and do not require the supernatural designer’s personal intervention. Is that right?

    Sure. My position is clear. We can infer design through functional complexity, and in no other way.

    The threshold is debatable. For the moment, I will stick to 150 bits (35 AAs). I will not make design inferences for lower functional complexities.

    However, my reasonable conviction is that Axe is right, and that the true edge of biological random evolution is about 5 AAs.

    Of course, the more the data, the more we can focus those issues.

    And please, take all the time you need.

  134. 134
    Piotr says:

    By the way, there’s an interesting discussion of biological “function” on Dan Graur’s blog. Very timely.

    One of the reasons why I’m so interested in the concept is that it has very close analogues in theories of language variation and change.

  135. 135
    gpuccio says:

    Piotr:

    “Do you mean that evolution is about to end soon, as new proteins get shorter and shorter? ;)”

    Maybe you are not serious here, but I really think that evolution will go on, but it will be mainly non protein evolution (non coding genes, regulatory elements, procedures).

  136. 136
    gpuccio says:

    Piotr:

    “One of the reasons why I’m so interested in the concept is that it has very close analogues in theories of language variation and change.”

    Obviously! That’s the first thing I thought when you said that you are a linguist.

    But let’s remember that language is born and changes in part because of conscious experiences. 🙂

  137. 137
    gpuccio says:

    Piotr:

    Well:

    “Because genomes are products of evolution rather than “intelligent design,” all genomes contain functional and nonfunctional parts. ”

    is not exactly a promising way to begin, at least for me. 🙂

  138. 138
    gpuccio says:

    Piotr:

    For your convenience, I will try to briefly sum up the concept of function in defining dFSCI:

    a) We have an object from which it is possible to objectively read some digital sequence according to some possible rule. Any rule can be applied, provided it is objectively stated, so that any observer can derive the same sequence with that rule.

    b) An observer can propose any possible function for the object with its sequence. What is a function? Simply a way we can use the object and its sequence to obtain some well defined result. Again, the function must be objectively defined, and the observer must give an objective way of measuring it, and if necessary a threshold to categorize it in binary form.

    c) For each function defined in that way, we can compute a functional complexity. If the function is referred to the digital sequence, the computation is easier (that’s why I use the dFSCI concept). It is essentially -log in base two of the ratio bewteen the number of functional sequences of that length and the number of possible sequences of that length (the target space/search space ratio).

    This is just the essential.

    Those concepts can be applied to any digital sequence: language, software, protein coding genes.

  139. 139
    Joe says:

    gpuccio- If Piotr knew anything about biology he wouldn’t be making the claims that he is making. Right now all we have is his say-so, which is meaningless regardless of what he does for a living- so you are correct and I was wrong.

  140. 140
    Joe says:

    OK I went to Dan Graur’s blog and found many bald declarations but nothing wrt an interesting discussion. As if I needed more evidence that Piotr is on an agenda.

  141. 141
    jerry says:

    As if I needed more evidence that Piotr is on an agenda.

    Most people who come here know only what the majority are saying and assume we are religious crackpots. After all there are some here who would qualify as such. i am sure Piotr is the same. He is a linguist and languages have definitely evolved over thousands of years. Also most people looks at dogs and other such animals and see how they come in very different physical shapes and assume that over million of years that natural processes could do the same.

    But he does not seem to understand that the information changes necessary for evolution are not as simple as that for languages or dog breeding. He seem to assume that small random changes will build the necessary proteins when we know it cannot. Most of the naturalists who come here assume that. Allen Fox till he disappeared here would constantly say that Axe and Durston were wrong. Fox would try to have a debate with Durston and tell him why his ideas and research were bogus.

  142. 142
    gpuccio says:

    Joe, jerry:

    Let us leave Piotr free to express his ideas. We are here to debate with those who think differently, after all.

    Piotr has been a good listener, until now, and at least the discussion has become specific and technical, which is always a good thing. Moreover, being a linguist, he could be more open-minded than a biologist. Let’s see.

    The worst that can happen is that we go on disagreeing, without even being able to understand why.

  143. 143
    Piotr says:

    @Jerry

    Sorry if you found my judgement of Wilcox’s talk too summary, but it’s really a lot of nonsense despite the “hundreds of references”. Please show me one research paper which claims that human regulatory networks are “incredibly more complex” than those of a chimpanzee (or any other mammal, for that matter). Are there any such reports among the numerous articles cited by Wilcox? I don’t think so.

    Nor do Wilcox’s theological preamble and the discussion of questions like the original sin further in the same presentation inspire much confidence in the quality of his biological argument. He also swallowed the ENCODE hype hook, line and sinker. Please, don’t expect me to take him seriously.

  144. 144
    Querius says:

    The worst that can happen is that we go on disagreeing, without even being able to understand why.

    I disagree. 😉 The worst thing is ad hominem attacks.

    I would ask Piotr what actually drives change in languages. Chance and necessity? Natural selection? A desire to alienate from another population? Changes in thought processes and cultural values?

    How would one be able to tell the difference between a synthesized language and a “natural” language?

    How do linguists judge common descent between languages? Is there a tree of life in language and did they all start from a single language as current OOL theories suggest in the realm of biology?

    Why does Latin seem more complicated than current Romance languages? What’s different between now than then?

    What evidence supports your assertion that there’s close analogues between biological evolution and the observed changes in languages?

    -Querius (a blend of query and curious)

  145. 145
    Piotr says:

    Let me begin with this one.

    How do linguists judge common descent between languages? Is there a tree of life in language and did they all start from a single language as current OOL theories suggest in the realm of biology?

    There is good evidence of relationship for some groups of languages. For example, English is related not only to German, Dutch and Swedish (which shared a common ancestor about 2000 years ago), but also — much more distantly — to Greek, Latin, Irish, Russian, Lithuanian, Hindi, Farsi, Armenian, Albanian, and many others within the so-called Indo-European family. There are many established language families: some with hundreds of members, some smaller, some consisting of a single language (for example, Basque).

    To judge common descent we use the so-called comparative method, which is not very different from what biologists do. In a nutshell, we look for demonstrable homologies. We don’t know at present if all extant languages are ultimately related. It’s a possibility, but we simply haven’t got enough information to prove long-range relationships. The known families consist of smaller units (also united by common ancestry), like Germanic, Slavic, Celtic, etc. There’s a lot of horizontal transfer (borrowing) between languages, which often has the effect of blurring genetic relationships in the long run.

    It’s a vast subject and I wouldn’t like to developp it here. Anyone interested in historical and evolutionary linguistics is welcome to my blog, where I discuss such things. I haven’t posted there for a few months, but intend to continue soon.

  146. 146
    Mapou says:

    What evidence supports your assertion that there’s close analogues between biological evolution and the observed changes in languages?

    Why would this be a plus for Darwinian evolution and not also for Design evolution? I think that hierarchical evolution makes perfect sense within the Intelligent design paradigm. Designs do evolve over time simply because designers come up with new designs that are strongly influenced by previous designs.

  147. 147
    jerry says:

    Please, don’t expect me to take him seriously.

    You have just pigeon holed yourself as not a serious commenter.

  148. 148
    gpuccio says:

    Mapou:

    I agree. Of course designers are strongly influenced by previous designs. There are logic connections, in biological design, which can be studied and analyzed, once the design paradigm is accepted.

    And, as already said, languages evolve with the constant influence of conscious beings.

  149. 149
    Upright BiPed says:

    We don’t know at present if all extant languages are ultimately related.

    Each and every one of them is indisputably related by the singular physical conditions by which they operate in the material world. These are precisely the same physical conditions as those found in the translation of the genetic code.

    I’m just aghast that a person with a background in language would not see the interest in this demonstrable fact.
    The unique process by which physical effects are produced from language and mathematics are found nowhere else in the cosmos except in the translation of the genetic code. A physical capacity that would not appear in the historical record (from our perspective) until the rise of humanity, was not only clearly present at the origin of life, but is the manifest physical reason life on this planet exists.

  150. 150
    Piotr says:

    @Upright Biped

    We all have the same language faculty (biologically grounded ability to learn and use a language). It doesn’t logically follow that all languages spoken today had a single common ancestor or that there was ever a time when the whole human population spoke one language. The former is barely possible (but far beyond our current ability to prove such a thing); the latter is highly unlikely.

    “Being related” has a concrete definition in linguistics: it means being demonstrably derived from a common ancestor, not just being a similar type of code. Perhaps you would not be so aghast if you’d had a little training in historical linguistics.

  151. 151
    Upright BiPed says:

    Piotr

    You should practice a little more disciplined reading comprehension. There is nothing I wrote that had anything to do with a single common linguistic ancestor. My comment was about the physical process. I think I made that most abundantly clear.

  152. 152
    Piotr says:

    @UB In that case I can’t see which part of what I’d written made you so aghast. Querius’s question was about determining common descent in linguistics (i.e., about common ancestors), so I simply replied to that. I did not declare any lack of interest in “physical processes”. So much for reading comprehension.

  153. 153
    Upright BiPed says:

    Piotr,

    While it’s true you”ve not “declared” a lack if interest in the physical properties I’ve brought up to you, but you’ve most certainly demonstrated it. Three days ago you declared on this forum that duplication and origin of life are separate topics. When I pointed out to you that they both are dependent on these same unique material conditions, you showed the same general disinterest then.

    That’s fine, you are not required to be curious. I’ll leave it alone.

  154. 154
    Querius says:

    Thank you for your comments to my questions, Piotr.

    Through a variety of circumstances, I’ve been exposed to several languages. I’ve always been fascinated by how different that they can be conceptually. For example, the Navajo language being so verb heavy.

    That you’re skeptical of a single origin of all languages might convey to you why some of us are skeptical of a single point of the origin of life.

    Do you think the most commonly used languages are evolving in complexity?

    -Q

  155. 155
    Mung says:

    Upright BiPed, what with Piotr being a linguist, you’re probably going to have to spell it out for him. 🙂

  156. 156
    Mung says:

    Is it somehow more probable that proteins should gain in length and function by adding additional “modules,” or that they simply arise de novo, and why?

  157. 157
    Joe says:

    Mung- Adding amino acids to an existing small protein would just block its substrate and render it useless. And long proteins require chaperones to find their functional shape.

    So unless the process is guided such that the simultaneous changes Axe discusses occur, it doesn’t have a chance of doing something useful.

  158. 158
    Mung says:

    Hi Joe,

    I tend to agree with your analysis. I intend to read that chapter (again?) in The Nature of Nature. But guided by what? According to YEC’s, God is not guiding these changes.

    So there’s no “intelligent design intervention” going on.

    Evolution does not require the guiding hand of God.

    Materialists and Atheists and YEC’s find common ground!

    What odd bedfellows =p

  159. 159
    Mung says:

    Joe, what I am trying to get you to understand, in my fumbling and no doubt irritating way, is that whether evolution is guided or not hardly matters if there is a mechanistic explanation.

  160. 160
    Mung says:

    Mung:

    How do young earth creationists explain ORFan genes?

    Joe:

    YECs explain ORFan genes by way of non-random evolution, ie “built-in responses to environmental cues” (Spetner 1997).

    Spetner:

    My speculation here is speculative. – p. 184

    Spetner:

    …nonrandom adaptive variation, arising from an environmental signal turning ON an already present set of genes, is hard to account for. – p. 191

    Spetner:

    I suggest that other organisms also may have latent parts of their genome dedicated to be adaptive to a certain set of environmental conditions that may arise. Then environment can then supply a cue that will turn ON the latent section that will make the organism adaptive. – p. 192

    This is not an explanation for ORFan genes. At best it assumes their existence rather than explaining their existence.

  161. 161
    Mung says:

    Joe quotes Douglas Axe from The Nature of Nature. There is no entry in the index for ORFan gene or orphan gene or taxonomically restricted gene.

    So far my reading of Spetner (quotes @ 160) offers no YEC explanation for orphan genes. Will the chapter by AXE likewise fail to provide the missing explanation?

  162. 162
    Mung says:

    Axe:

    The elucidation of the genetic code in the late 1960’s provided a precise framework for understanding the effects of genetic mutations on protein sequences.

    …The code had made it clear that the vast set of possible proteins, each of which could conceivably be constructed by genetic mutations, is far too large to have actually been sampled to any significant extent in the history of life.

    What is the implication for the origin of orphan genes?

  163. 163
    gpuccio says:

    Mung:

    The implication is the same both for orphan genes and for any other protein, orphan or not:

    Any protein of some functional complexity, when it appears for the first time, with sequence, structure and function unrelated to what already exists (which is true for at least the 2000 superfamilies in SCOP), cannot be explained neither by random processes of variation (any kind of random variation) nor by any known algorithm (like NS). The only possible explanation is guided variation by design.

    Quite an implicaton, I would say.

  164. 164
    Joe says:

    OK Mung, seeing that you are trapped in a box, then it is MY “built-in responses to environmental cues” that builds ORFan genes.

    Unbelievable that you just cannot extend Spetner’s ideas to include orfan genes.

    Orfans were found in 1996 and the book was already written and on its way to publication

  165. 165
    AVS says:

    “Adding amino acids to an existing small protein would just block its substrate and render it useless.”

    You sure about that Joe, or are you just talking out of your rear-end?

  166. 166
    Piotr says:

    I was also going to ask Joe if new proteins necessarily required new chaperones (or maybe some of those already available could do, eh?). I leave aside the question if chaperones actually help proteins “to find their functional shape”, since it isn’t quite the issue here.

  167. 167
    Piotr says:

    @Querius:

    That you’re skeptical of a single origin of all languages might convey to you why some of us are skeptical of a single point of the origin of life.

    We go where the evidence leads us. There is good evidence of universal common descent in biology, and there is good evidence of partial common descent in linguistics.

    Sometimes we manage to assign more members to an already established linguistic family. For example, Indo-European has grown since the 19th century because a couple of new branches (Anatolian and Tocharian) were discovered, both of them branching off at the root of the family-tree.

    The Semitic family (whose members are Hebrew, Phoenician, Arabic, Aramaic, Amharic and Akkadian, among others) is now regarded as part of a much larger genetic unit, including also Old Egyptian as well as several language groups in the Sahara and Sahel regions of North Africa (Berber, Cushitic, Chadic, and more speculatively Omotic). We call this extended “superfamily” Afroasiatic.

    But still there are scores of families (from tiny ones to giants with hundreds of members) whose external relationships remain unknown at present.

    Do you think the most commonly used languages are evolving in complexity?

    The “overall” complexity of a language is hard to define and measure. Of you look at its various components, like phonology, syntax, lexicon, and inflectional or derivative morphology, their complexity may increase or decrease historically.

    For example, Modern English has lost nearly all the declensional and conjugational endings still used in Old English, but its syntax has become more complicated in some ways, e.g. thanks to the development of structures like the complex tenses (not only I write and I wrote, but also I have written, I will be writing, I would have been writing, etc.). They were not deliberately “designed” by anybody in one fell swoop, but appeared gradually and became grammaticalised slowly over the centuries until they settled into a stable system (as recently as 300 years ago a construction like the road is being repaired would have been considered ungrammatical). And of course the lexicon of Modern English has grown enormously since the Middle Ages, mostly through borrowing.

  168. 168
    Querius says:

    Piotr,

    Thanks for your explanation.

    . . . and there is good evidence of partial common descent in linguistics.

    I don’t understand how common descent could be partial. Are you saying that all human languages started from a single common source, but later somehow branched into major families, and were subsequently modified by common use and disuse, borrowing, and innovation?

    I was once told by a colleague that a scientist of our acquaintance chose to learn Turkish, because he considered it nearly a perfect synthetic language. In your opinion, why might he have concluded this, or would you disagree?

    Just curious, that’s all.

    -Q

  169. 169
    Piotr says:

    I don’t understand how common descent could be partial. Are you saying that all human languages started from a single common source, but later somehow branched into major families, and were subsequently modified by common use and disuse, borrowing, and innovation?

    No, I mean that we don’t know if there was a single source. We start with modern and historically documented languages and classify them in the same family if we have evidence of relationship. There are, for instance, 400+ Indo-European languages, and we can demonstrate they had a common ancestor a few thousand years ago. There are 30+ Turkic languages, and they are also descended from a common ancestor. But we do not know “beyond reasonable doubt” if the Turkic and Indo-European families go back to a single historical source.

    That’s why I call this kind of common descent “partial”, not “universal”. Given the limited evidence that we have, we can reconstruct many common ancestors — one for each family — but not a single one for all of them.

    Note that people have probably used languages for hundreds of millennia, but writing was invented little more than 5000 years ago, and our best reconstructive methods reach back possibly twice as deep. We can probe only a thin slice of the total history of spoken language.

    I was once told by a colleague that a scientist of our acquaintance chose to learn Turkish, because he considered it nearly a perfect synthetic language. In your opinion, why might he have concluded this, or would you disagree?

    A “synthetic” language is one in which a word typically contains many morphemes, while an “isolating” language prefers words that can’t be decomposed into morphemes. Chinese is an extreme example of the latter, but there’s actually a continuum of types rather than a clearcut isolating vs. synthetic dichotomy. One could say that Turkish is more synthetic than English, but there are languages with a still higher morpheme/word ratio. Has your friend considered learning Eskimo or Cherokee?

  170. 170
    Mung says:

    Joe:

    Unbelievable that you just cannot extend Spetner’s ideas to include orfan genes.

    There’s certainly nothing in Spetner that would lead me to extend his ideas to include orphan genes. In fact, having completed my re-reading of his chapter seven, his NREH (nonrandom evolutionary hypothesis) precludes me from doing so.

  171. 171
    Mung says:

    Figure 1 shows the distribution of protein chain lengths for all proteins known to be involved in enzymatic functions in E. coli, either alone or in combination with other proteins. The mode of the distribution shows that the most common length of these proteins is around 300 amino acid residues, with the higher mean and median lengths reflecting the existence of numerous protein chains that are much longer than this.

    – Douglas Axe. The Nature of Protein Folds: Quantifying the Difficulty of an Unguided Search Through Protein Space

  172. 172
    Mung says:

    AVS:

    You sure about that Joe, or are you just talking out of your rear-end?

    Well, at least we now know where your ear is.

    Joe:

    Doug Axe goes over this in his essay in “The Nature of Nature” see catalase (for example)

    Well joe, perhaps AVS has never heard of Douglas Axe and just can’t be bothered to spend the time or money to become familiar.

    Reminds me of his demand that I debate him over the contents of a book he can’t be bothered to read.

  173. 173
    gpuccio says:

    Piotr and all:

    Stimulated by the discussion here, I have just made a post on functional information.

  174. 174
    Mung says:

    A quote for Upright BiPed:

    The linkage of an amino acid to a tRNA is crucial for two reasons. First, the attachment of a given amino acid to a particular tRNA establishes the genetic code.

    Aminoacyl-Transfer RNA Synthetases Read the Genetic Code

    gpuccio, I am lazy and don’t want to read through your past posts 🙂

    Did you bring up aminoacyl-tRNA synthetase?

    How short are they, how specific are they, how important are they, what are their precursors?

  175. 175
  176. 176
    gpuccio says:

    Mung:

    I have always brought up aminoacyl-tRNA synthetases! I (like UB) am a big fan of aminoacyl-tRNA synthetases (or, more correctly, ligases).

    They are 20 wonderful molecules, divides in two classes. And they are long, big and complex. And, obviously, they have no precursors.

    Here are some lengths in humans:

    Class I:

    Arginine: 660 AAs
    Cysteine: 748 AAs
    Leucine: 1176 AAs

    Class II:

    Alanine: 968 AAs
    Asparagine: 548 AAs
    Glycine: 739 AAs

    They are old molecules, obviously. Even their “evolution” after their appearance is perplexing, and there are many problems, usually intepreted as HGT.

  177. 177
    AVS says:

    Funny Mungy, although my point is that Joe is wrong for the most part. For starters, there is really no such thing as a “small” protein enzyme. Catalase is relatively small, and yet is made up of multiple subunits, each over 50kDa.

    Also, “adding amino acids” is just about as likely to either HAVE an effect, or NOT HAVE an effect, on substrate binding. In fact, in the lab, proteins are often expressed with entire fluorescent protein constructs engineered into their sequence and they still function properly the majority of the time.

    I’m still waiting for the info that “refuted” me from that book by the way. =)

  178. 178
    Mung says:

    They are old molecules, obviously.

    exactly!

    You don’t get proteins without them, you don’t even get protein domains without them.

    All this talk of how proteins can evolve from short sequences into longer sequences doesn’t seem to mean much if it cannot explain them.

  179. 179
    Querius says:

    Piotr @ 165 explained

    One could say that Turkish is more synthetic than English, but there are languages with a still higher morpheme/word ratio. Has your friend considered learning Eskimo or Cherokee?

    Thank you. I’ve lost touch with him, but I’ve always wondered about the structures and capabilities of different languages.

    Would you say that that languages came into being purely by chance or is it more likely that they have intelligence as their source? I was just reminded that children sometimes invent their own languages.

    -Q

  180. 180
    gpuccio says:

    Piotr:

    Thank you for your beautiful explanations about languages. That is really a fascinating discipline.

    My view about the evolution of languages s that it is a special kind of designed process, in the sense that it is the result of multiple design acts by multiple designers. And, obviously, many random or algorithmic processes influence the results too. But language comes from intelligent conscious beings, and is mainly the result of understanding and purpose. IOWs, of design.

  181. 181
    gpuccio says:

    Piotr:

    I have just seen that in your blog there is a discussion on function which has interesting connections with my post on functional information. Let me say that I did not copy the example of the stone from your post there: I read it only now. 🙂

  182. 182
    Mung says:

    AVS:

    I’m still waiting for the info that “refuted” me from that book by the way. =)

    Um, no. You’re not.

    You’ve already admitted that “it’s all just chemistry.”

    Now when you finally manage to get your grubby little penny-pinching paws on a copy of that book, perhaps from your local university library, you can show us how it contradicts your assertion that “it’s all just chemistry.”

    But don’t expect me to hold my breath.

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