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ICC 2013: Paul Nelson’s Keynote Address

What would count as evidence against common descent given that organisms share such strong similarities? Darwin for the sake of argument assumed that the Creator (presumably God) created life, but argued the data accorded better with universal common ancestry. Nelson contested that view in his keynote address by arguing that if the principle of continuity is violated, there is no need to assume common ancestry. That even if a pair of organisms are 90% similar, that 10% difference could be sufficient to falsify common ancestry if the gap in differences are sufficiently large to be bridged by mindless processes.

IF it could be demonstrated that any complex organ existed, which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down.

Charles Darwin

But orphans are exactly that sort of “complex organ”, hence Darwinism has been falsified on Darwin’s own terms.

There are ID proponents who accept common descent, but a large fraction of ID proponents accept special creation. Strictly speaking, rejection of common descent does not necessarily imply ID, but it does make ID more believable for most people…

So how much difference is needed to challenge common descent? Consider if you had 90% of the characters correct in a 5000 character cryptographic key, is it reasonable to assume chance processes will resolve the final 10%? It is probably very easy to make a biological organism 10% different from another in terms of destructive processes, but not so easy in terms of constructive process since new protein systems are like new login/password, lock-and-key systems.

Nelson’s keynote highlighted the problem of orphan genes and presented them as evidence against common descent. To understand more about the orphan gene problem, visit A new mechanism of evolution — POOF.

Nelson pointed out that it was hoped that more sequencing would find the missing ancestors of the orphan genes which had looked like they poofed into existence. It was hoped the appearance of a POOF in the history of life was an illusion resulting from our lack of data, and that we would eventually find missing links for the orphans. But that has not happened, the gaps only have gotten worse the more we learn, and the trend is that we will discover more orphans as we sequence more organisms. That means we will find even more missing links, and that argues against common descent of those orphans, and by way of extension common descent of the organisms.

Nelson pointed out Ventner, Woese, Doolittle and others are skeptical of the need of common descent in light of these developments.

We cannot expect to explain cellular evolution if we stay locked in the classical Darwinian mode of thinking…

The time has come for biology to go beyond the Doctrine of Common Descent.

Carl Woese

When Nelson made some of his bold claims about orphans, it was when the Genbank numbers were small in the 90s. That’s all changed. The best graph available goes to 2007, and it has since grown even more.

Nelson made a testable prediction that has been borne out by observation. Congratulations!

Nelson highlighted papers such as this one Orphans as taxonomically restricted and ecologically important genes.

This paper shows that a persistent pattern in biology of lots of species specific orphans will continue to be found in each organism, maybe 10% for one prospective data set:

A similar pattern can be seen for D1 where 10 % of all predicted coding regions in 200 species are predicted to be orphans.

How widespread will the pattern be as we sequence more organisms? Here is a problem:

These trends reveal several interesting points. First, given our current dataset for bacteria, it is not possible to make an estimate of the maximum number of orphans, as orphan growth does not show evidence of reaching a plateau. This conclusion is also supported by examining the rate at which new protein families are discovered (Kunin et al., 2003).

Second, it appears that improved taxonomic sampling of distantly related genomes is continuing to reveal large numbers of orphans. These data suggest that the number of bacterial orphan genes will continue to increase for the foreseeable future as long as we continue to assay novel branches of the microbial tree of life. Therefore, although improved taxonomic sampling is reducing the overall percentage of orphans, it cannot be used to assign all orphans to known gene families. Furthermore, it is also likely that orphans will continue to be found in lineages that have already been heavily sampled (Hayashi et al., 2001; Perna et al., 2001).

Creationist translation: more evidences against common ancestry will emerge. Orphans are important because if they have no ancestor, then arguments of slow gradual evolution of proteins from pre-existing proteins is falsified, and the numbers developed by Axe and Gauger become immune to complaints that they aren’t considering similarly functioning proteins since in the case of orphan proteins, similar pre-existing proteins do not exist. POOF becomes the only recourse.

In addition to the above study, here is another one:

Orphan genes are defined as genes that lack detectable similarity to genes in other species and therefore no clear signals of common descent (i.e., homology) can be inferred. Orphans are an enigmatic portion of the genome because their origin and function are mostly unknown and they typically make up 10% to 30% of all genes in a genome

http://gbe.oxfordjournals.org/content/5/2/439.abstract

Strictly speaking orphans don’t completely disprove common descent of entire creatures, but it does cast doubt on the common descent of orphans. But supposing 10-30% of genomes had to have been poofed into sudden existence, why not the whole organism? If POOF works as an explanation for 10-30%, why not 100%? That would seem more parsimonious if one accepts, as Darwin did for the sake of argument, that there is a Creator.

For sure there are deep similarities between humans and other creatures, but there are also differences. Evolutionists have made suspect claims of the degree of similarity (see: WD40 som fish are more closely related ot you than they are to tuna and ICC 2013 Jeff Tomkins vs evolutionary biologist who got laughed off stage).

The question then arises, supposing God is the Creator, despite some acute differences, why then did He did he also make creatures so similar? Subject of perhaps of another discussion. :wink:

NOTES
1. Paul Nelson is one of the few YECs well-respected in both YEC and ID circles. He is the grandson of Byron C. Nelson a theology graduate of Princeton who argued against the damaging effects of Darwinism on society. Paul Nelson has compiled the writings of his grandfather here: The Creationist Writings of Byron C. Nelson

2. Three Byron C. Nelson awards were given at ICC 2013 to Steve Austin, John Baumgardner, and Russell Humphreys.

3. photo credits

http://www.ncbi.nlm.nih.gov/core/assets/genbank/images/genbankgrowth.jpg

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34 Responses to ICC 2013: Paul Nelson’s Keynote Address

  1. But supposing 10-30% of genomes had to have been poofed into sudden existence, why not the whole organism?

    That’s 10-30% genes within the genome. I’ve made that mistake myself.

    Just as a thought experiment… since morphologies are just various assemblages made by protein-coding genes, what would we say if we found a significant and consistent amount of homology-free morphology on all animals? (e.g. 10-30% homology-free bone structure)

    Another question.. why are orphan gene levels consistently averaging around 10-30% ? This seems like a strange result of a directionless process. Why aren’t there swathes of populations whose journey on the mystical fitness landscape never benefited from the poof-development of orphan genes? Why such a non-random (and non-homologous) pattern emerging out of supposedly millions of years of blind development of biodiversity?

    Also.. since fully novel poof-genes seem to be an unavoidable occurrence within relatively short periods of evolutionary time, why could we not expect to observe poof-genes emerging in the studies of tens of thousands of generations of “evolving” bacteria populations?

  2. Why such a non-random (and non-homologous) pattern emerging out of supposedly millions of years of blind development of biodiversity?

    To clarify…

    Natural Selection is claimed to be the non-random component, filtering random mutations.

    Selection could not have been playing any role with the non-functional sequences making up future orphan genes, because the sequences are not conserved between species.

    So why are there apparently non-random quantities of orphan genes across existing biodiversity?

    That is to say… why are there apparently non-random quantities of events where non-conserved, random genetic sequences became functional across existing biodiversity?

  3. Allegedly ORFans arose basically by chance, for example via recombination, and possibly helped lead to the divergence from the parent population.

  4. I thought we agreed a week or so ago that no one knows if ORFan are really genes? What are they coding for? Until that is known then all the discussion is just speculation, isn’t it?

    Also anything definitive would have to wait till there is a comparison between the genomes of various distant ethnic groups. For example, what are the similarities/dissimilarities between Australian aborigines and South American Indians, Africans, Europeans? The aborigines have been in Australia for about 40,000 years and some of the South American Indians have been there for 15,000 years. Do they all have the same ORFans?

    I just got back the first cut at my genome by 23andme and it said I had 3% Neanderthal genes. I joked with my wife that she better get me a club for my birthday. Then I read that most people in the world have between 2 and 4 % Neanderthal genes except for Africans who have none. The Neanderthal supposedly died out about 25,000 years ago.

    Until we can compare various groups from around the world on these so called ORFan genes or know if they code fro anything meaningful then we are just speculating.

    Maybe 23andme will publish some of their findings. I only think they analyze a small percentage of everyone’s genome but they potentially have a huge database.

  5. Lifespy,

    Good questions. If you look into it you’ll find, contra the claims in this post, that the distribution of ORFans in animal genomes at least is not all consistent. In fact, there’s a very clear phylogenetic pattern with species for which there is a closely-related genome sequence having less ORFans. As we keep filing those gaps we can expect ORFans to vanish.

    What will be more interesting is how lineage-specific genes arise.

  6. Jerry,

    There are at least some genes that actually do something that are human-specific. But you are right, it’s likely many ORFans discovered in silico will turn out to be random gene-like sequences (genomes are big, they have to have some of these)

  7. Jerry, wd400, apparently quite a few orphans have been found to be protein-coding across a diverse amount of species. I haven’t tracked down these specific studies yet, though.

    …But as the genomes of more and more organisms were sequenced, genetic family reunions proved to be the exception rather than the rule. Orphan genes have since been found in every genome sequenced to date, from mosquito to man, roundworm to rat, and their numbers are still growing. The study of orphan genes is still in its infancy, and we know very little about most of them.

    Those we do know about are a mixed bag. Some are involved with the repair and organisation of DNA, or in controlling the activity of other genes. The insect orphan flightin, which encodes a muscular wing protein, evolved to aid flight. And in a study published last year, Manyuan Long of the University of Chicago and his team showed that two recently evolved young insect orphans help shape foraging behaviour in the fruit fly Drosophila.

    In corals, jellyfish and polyps, orphan genes guide the development of explosive stinging cells, sophisticated structures that launch toxin-filled capsules to stun prey. In the freshwater polyp Hydra, orphans guide the development of feeding tentacles around the organism’s mouth. And the polar cod’s orphan antifreeze gene enables it to survive life in the icy Arctic.

    http://ccsb.dfci.harvard.edu/w.....n_2013.pdf

  8. Yeah. There is no doubt that there are orphan genes. But it’s also clear that these are not all species-specific genes. Rather, part of their orphan-ness is an artifact of the particular genomes we’ve sequenced. Both the papers Sal links to show this, through the phylogenetic pattern in the insect paper, and explicitly in Figure 1b on the bacterial genome paper.

    It’s probably better to think of ‘orphans’ as lineage specific genes then (that’s what the microbe paper suggests). Only that would make orphan genes evidence for common descent…

  9. Contrary to wd400′s assertion,

    It’s probably better to think of ‘orphans’ as lineage specific genes

    we have clear evidence for species specific orphan genes in humans as even arch Neo-Darwinist Coyne admits:

    “More than 6 percent of genes found in humans simply aren’t found in any form in chimpanzees. There are over fourteen hundred novel genes expressed in humans but not in chimps.”
    Jerry Coyne – ardent and ‘angry’ neo-Darwinist – professor at the University of Chicago in the department of ecology and evolution for twenty years. He specializes in evolutionary genetics (and inquisition style censorship).

    And it is held that these orphans make Darwinian evolution more untenable than it already was:

    Proteins and Genes, Singletons and Species – Branko Kozuli? PhD. Biochemistry
    Excerpt: Horizontal gene transfer is common in prokaryotes but rare in eukaryotes [89-94], so HGT cannot account for (ORFan) singletons in eukaryotic genomes, including the human genome and the genomes of other mammals.,,,
    The trend towards higher numbers of (ORFan) singletons per genome seems to coincide with a higher proportion of the eukaryotic genomes sequenced. In other words, eukaryotes generally contain a larger number of singletons than eubacteria and archaea.,,,
    That hypothesis – that evolution strives to preserve a protein domain once it stumbles upon it contradicts the power law distribution of domains. The distribution graphs clearly show that unique domains are the most abundant of all domain groups [21, 66, 67, 70, 72, 79, 82, 86, 94, 95], contrary to their expected rarity.,,,
    Evolutionary biologists of earlier generations have not anticipated [164, 165] the challenge that (ORFan) singletons pose to contemporary biologists. By discovering millions of unique genes biologists have run into brick walls similar to those hit by physicists with the discovery of quantum phenomena. The predominant viewpoint in biology has become untenable: we are witnessing a scientific revolution of unprecedented proportions.
    http://vixra.org/pdf/1105.0025v1.pdf

    But to more effectively demonstrate the incoherence of wd400′s neo-Darwinian position, let’s take a look at the overall point of what Darwinists are actually trying to claim in their ‘bottom up’ approach. The claim that changes in genotypes (genes) generate changes in phenotypes (body plans). These following quotes illustrate the main problem being revealed with the ‘bottom up’ Darwinian scenario:

    Why the ‘Gene’ Concept Holds Back Evolutionary Thinking – James Shapiro – 11/30/2012
    Excerpt: The modern concept of the genome has no basic units. It has literally become “systems all the way down.” There are piecemeal coding sequences, expression signals, splicing signals, regulatory signals, epigenetic formatting signals, and many other “DNA elements” (to use the neutral ENCODE terminology) that participate in the multiple functions involved in genome expression, replication, transmission, repair and evolution.,,,
    Conventional thinkers may claim that molecular data only add details to a well-established evolutionary paradigm. But the diehard defenders of orthodoxy in evolutionary biology are grievously mistaken in their stubbornness. DNA and molecular genetics have brought us to a fundamentally new conceptual understanding of genomes, how they are organized and how they function.
    http://www.huffingtonpost.com/.....07245.html

    HOW BIOLOGISTS LOST SIGHT OF THE MEANING OF LIFE — AND ARE NOW STARING IT IN THE FACE – Stephen L. Talbott – May 2012
    Excerpt: “If you think air traffic controllers have a tough job guiding planes into major airports or across a crowded continental airspace, consider the challenge facing a human cell trying to position its proteins”. A given cell, he notes, may make more than 10,000 different proteins, and typically contains more than a billion protein molecules at any one time. “Somehow a cell must get all its proteins to their correct destinations — and equally important, keep these molecules out of the wrong places”. And further: “It’s almost as if every mRNA [an intermediate between a gene and a corresponding protein] coming out of the nucleus knows where it’s going” (Travis 2011),,,
    The question is indeed, then, “How does the organism meaningfully dispose of all its molecules, getting them to the right places and into the right interactions?”
    The same sort of question can be asked of cells, for example in the growing embryo, where literal streams of cells are flowing to their appointed places, differentiating themselves into different types as they go, and adjusting themselves to all sorts of unpredictable perturbations — even to the degree of responding appropriately when a lab technician excises a clump of them from one location in a young embryo and puts them in another, where they may proceed to adapt themselves in an entirely different and proper way to the new environment. It is hard to quibble with the immediate impression that form (which is more idea-like than thing-like) is primary, and the material particulars subsidiary.
    Two systems biologists, one from the Max Delbrück Center for Molecular Medicine in Germany and one from Harvard Medical School, frame one part of the problem this way:
    “The human body is formed by trillions of individual cells. These cells work together with remarkable precision, first forming an adult organism out of a single fertilized egg, and then keeping the organism alive and functional for decades. To achieve this precision, one would assume that each individual cell reacts in a reliable, reproducible way to a given input, faithfully executing the required task. However, a growing number of studies investigating cellular processes on the level of single cells revealed large heterogeneity even among genetically identical cells of the same cell type. (Loewer and Lahav 2011)”,,,
    And then we hear that all this meaningful activity is, somehow, meaningless or a product of meaninglessness. This, I believe, is the real issue troubling the majority of the American populace when they are asked about their belief in evolution. They see one thing and then are told, more or less directly, that they are really seeing its denial. Yet no one has ever explained to them how you get meaning from meaninglessness — a difficult enough task once you realize that we cannot articulate any knowledge of the world at all except in the language of meaning.,,,
    http://www.netfuture.org/2012/May1012_184.html#2

    Moreover,,

    With a Startling Candor, Oxford Scientist Admits a Gaping Hole in Evolutionary Theory – November 2011
    Excerpt: As of now, we have no good theory of how to read [genetic] networks, how to model them mathematically or how one network meshes with another; worse, we have no obvious experimental lines of investigation for studying these areas. There is a great deal for systems biology to do in order to produce a full explanation of how genotypes generate phenotypes,,,
    http://www.evolutionnews.org/2.....52821.html

    In fact, there is No Evidence For Body Plan Morphogenesis From Embryonic Mutations,,,

    Darwin or Design? – Paul Nelson at Saddleback Church – Nov. 2012 – ontogenetic depth – 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/

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

    Thus, despite the arrogant confidence that many Darwinists have in their bottom up Darwinian approach of genotype generates phenotype, the fact of the matter is that such confidence is severely misplaced since it is in fact ungrounded in empirical support.,, As to a glimpse of ‘top down’ control of body plans that was recently revealed and that was completely unanticipated by Darwinists, this following video is a ‘jaw dropper’:

    An Electric Face: A Rendering Worth a Thousand Falsifications – September 2011
    Excerpt: The video suggests that bioelectric signals presage the morphological development of the face. It also, in an instant, gives a peak at the phenomenal processes at work in biology. As the lead researcher said, “It’s a jaw dropper.”
    https://www.youtube.com/watch?v=wi1Qn306IUU

    Thus despite the denial of Darwinists, the last few years of advances in molecular biology have seen new evidences come forth on many fronts that have severely eroded the explanatory power of the ‘bottom up’ Darwinian theory.

    Verse and Music;

    139:13-14
    For you created my inmost being;
    you knit me together in my mother’s womb.
    I praise you because I am fearfully and wonderfully made;
    your works are wonderful,
    I know that full well.

    Life Got You Down? Just Remember You Got Thumbs! – video
    http://www.youtube.com/watch?v=_s8y9a12saU

  10. This tick species has 70% orphan genes.


    Why so many unknown genes? Partitioning orphans from a representative transcriptome of the lone star tick Amblyomma americanum

    Gibson et al 2013

    Expressed sequence tags (ESTs) were derived from different life stages and populations of A. americanum and combined with ESTs available from GenBank to produce 14,310 ESTs, over twice the number previously available. The vast majority (71%) has no sequence homology to proteins archived in UniProtKB. We show that poor sequence or assembly quality is not a major contributor to this high representation by orphan genes. Moreover, most unannotated sequences are functional: a microarray experiment demonstrates that 59% of functional ESTs are unannotated. Lastly, we attempt to further annotate our EST dataset using genomic datasets from other members of the Acari, including Ixodes scapularis, four other tick species and the mite Tetranychus urticae. We find low homology with these species, consistent with significant divergence within this subclass.

    http://www.biomedcentral.com/1.....5/abstract

  11. wd400,

    It’s probably better to think of ‘orphans’ as lineage specific genes then (that’s what the microbe paper suggests). Only that would make orphan genes evidence for common descent…

    That is interesting reasoning, considering orphans are defined by a total lack of any trace of common descent.

    I suppose they are lineage-specific in the sense that that humans come from a lineage of humans, and dogs come from a lineage of dogs.

  12. It seems that we know very little about ORFans. How many are there? People are saying a lot, in the tens of thousands. That would be consistent with current evolutionary thinking which says all the genome is subject to mutation. Lots of new genetic information but the chance of any of them producing useful proteins is not consistent with what Durston and Axe are saying.

    How many of the ORFans are transcribed? We don’t know but speculate it is a lot but no evidence of the number. Or is there evidence?

    How many are translated? Only a handful are mentioned. We seem to know that a few have useful functions.

    My guess is that this will clarify itself over the years and should be interesting to watch. And for the useful ones, it will be interesting to see how they could arose. Could any of Alan MacNeill’s famous ways of producing new information in the genome be responsible?

    Also we can see the shift away from the genome to the zygote itself as the storage bin of information for the organism’s structure. How is the zygote changed by natural processes? Not very likely according to Meyer or Nelson.

    All I am doing is trying to clarify what is known and a little bit of speculation too.

  13. Salvador:

    That even if a pair of organisms are 90% similar, that 10% difference could be sufficient to falsify common ancestry if the gap in differences are sufficiently large to be bridged by mindless processes.

    I think your meaning (assuming I understand your meaning) would be clearer if you said:

    “…if the gap in differences is too large to be bridged…”

  14. Lifespy,

    As that paper says, the tick has so many “orphan” genes partly because there are no genomic resources for any of it’s close relatives. In time, more will be sequenced and orphans will find relatives.

    Which is the point, really. Humans are a linage, sure, but so are primates. If we had only the human genome and no gorilla, chimp or orang, then there would be many more “orphans” in our genome. The phylogenetic pattern to orphan genes, with less present in those species for which a closely-related genome is avaliable, is yet more evidence for common descent.

  15. wd400

    As that paper says, the tick has so many “orphan” genes partly because there are no genomic resources for any of it’s close relatives. In time, more will be sequenced and orphans will find relatives.

    I don’t doubt lack of data as a factor, but that is invoking a pretty big coincidence if the majority of genes sequenced just happened to be orphans. And they were compared with other closely related tick species which had more well represented genomic data.

    Additionally, we reveal up to 5,261 functional genes for which no arthropod or tick homologs are currently available… Finally, low homology to I. scapularis and T. urticae, the closest arthropod species with significant genomic resources, showed that taxonomic isolation may contribute significantly to the high representation of unknown genes in the A. americanum library.
    http://www.biomedcentral.com/1471-2164/14/135

    Which is the point, really. Humans are a linage, sure, but so are primates. If we had only the human genome and no gorilla, chimp or orang, then there
    would be many more “orphans” in our genome.

    I don’t know that this is true at all, since Human orphan genes aren’t known to be any more similar to chimps than to frogs. By what reasoning do you claim subtracting chimp genomes will result in more orphan genes in humans? How many exclusive “Chimp-Human” orphans are there?

    The phylogenetic pattern to orphan genes, with less present in those species for which a closely-related genome is avaliable, is yet more evidence for common descent.

    Then aren’t you using the assumption that orphan levels represent phylogenetic distance as evidence for it at the same time?

  16. Then aren’t you using the assumption that orphan levels represent phylogenetic distance as evidence for it at the same time?

    No. It’s a clear finding of the insect paper Sal linked to in the OP.

  17. … I should say, it’s also way that quoted passage is saying by using the term “taxonomic isolation”. Acari are a huge and diverse subclass with many many more species than all mammals put together.

  18. How many exclusive “Chimp-Human” orphans are there?

    According to orthoDB and considering only great apes, ~450. Rather more than there are, Chimp-Gorilla orphans… which is interesting don’t you think?

  19. lifepsy:
    Then aren’t you using the assumption that orphan levels represent phylogenetic distance as evidence for it at the same time?

    wd400:

    No. It’s a clear finding of the insect paper Sal linked to in the OP.

    … I should say, it’s also way that quoted passage is saying by using the term “taxonomic isolation”. Acari are a huge and diverse subclass with many many more species than all mammals put together.

    It appears the researchers are using the same assumption as evidence. The level of orphan genes are used as the evidence for level of divergence.

    “We predicted that the percent matching between A. americanum ESTs and I. scapularis genomic datasets would be substantially higher than the percent matching to the UniProtKB database… the majority of A. americanum ESTs was found to have no match to UniProtKB proteins and no homology to I. scapularis genome, peptide, or EST sequences. This result supports a substantial degree of divergence between Ixodes and Amblyomma sequences.”

    The other hypothesis is that evolution didn’t happen.

    How many exclusive “Chimp-Human” orphans are there?

    According to orthoDB and considering only great apes, ~450. Rather more than there are, Chimp-Gorilla orphans… which is interesting don’t you think?

    Sorry, I don’t know how to navigate that database. Are you saying there are 450 gene sequences found only in Chimps and Humans that have no trace of homology to anything else? I’ve never heard anyone make that claim before.

  20. Lifespy,

    The tick paper is suggesting the lack of homologous sequences arises from their tick speicies phylogenetic isolation. The insect genome paper Sal linked to in the orginal post here very clearly shows a pattern w/ less orphan genes in those species that have a close relative with genomic resources.

    OrthoDB indeed lists ~450 genes that, among great apes, are known only form humans and chimps. The actual number you get from any attempt to isolate these sorts of lineage-specific genes is going depend on the particular methodology, and that database probably isn’t the best way to go.

    If someone like Nelson or Sal, who are trying to make something out orphan genes, wants to test that idea it would be relatively straight forward. Download the refseq proteins from human, and BLAST them against nr while excluding primate proteins. Now, blast the apparent “orphans” (i.e. proteins with no hits) against, in order, Macaque, Organ, Gorilla and Chimp genomes. Would take some time, but it’s not a hard analysis to run.

  21. I’m quite aware of what orthology means, Mung.

    In this case, Sal and others seem to think the presence or orphan genes is evidence against common descent. That argument is undercut but the fact these genes show a distinct phylogentic pattern. If there are ~450 genes that orthologous between human and chimp but not present in other great apes that’s (a) ~450 genes we’d call oprhans if we didn’t have the chimp genome and (b) evidence that some new genes arose in the human-chimp common ancestor after it diverged from gorillas.

    As I say, orthoDB is probably not the best tool for these analyses – but it would be easy for someone who is trying to make something out of the orphan genes to look and see whether lineage-specific genes meet the phylogenetic expectation.

  22. So, I might not have been very clear so far.

    There are two phylogenetic patterns here. The first, when we look at taxa that have not many genomic resources, is that there are more apparent orphans in those species that are distantly related to one with a sequenced genome. That’s evidence that a gene being “species specific” orphan is often an artifact of our own understanding.

    The second point I’ve been trying to make is about lineage-specific to genes. Those known only from a few species (and that would be considered “orphans” if we didn’t have the other genomes). If de-novo genes arise in simple-ish fashion, we should expect there to be a few genes restricted to humans and chimps, a few others to humans, chimps and gorillas and so on. There should be rather less genes restricted to gorillas and chimps but present in humans (presuming gene loss from one species is unlikely).

    I actually doubt there would be 400 human-chimp restricted genes. Because the time for them to evolve would be pretty short – the gap between the (human-chimp)-(gorilla) speciation was short enough that we are more similiar to gorillas for some of our genes than to chimps.

    As I say, someone with a little knowhow could do all the comparisons and it would be interesting to see what the numbers come out to be.

  23. But isn’t that precisely what you were arguing until I pointed out the problems with such a position?

    I wasn’t arguing anything, I was asked how many human-chimp “orphans” their might be, and orthoDB was the first approach to that question that poped into my brain. There are many more Human-Chimp specific genes than Chimp-Gorilla specific ones.

    As I have said, it would be interesting to see how primate-specific genes are distributed among the ape lineages. Almost every time someone looks at orphans in detail they end up finding an origin for most of them

  24. Saying that humans and chimps shared a common ancestor is not science because it cannot be tested. And that is regardless of any ORFan genes.

  25. wd400,

    The tick paper is suggesting the lack of homologous sequences arises from their tick speicies phylogenetic isolation. The insect genome paper Sal linked to in the orginal post here very clearly shows a pattern w/ less orphan genes in those species that have a close relative with genomic resources.

    Even if this turns out to be true (and it pretty much sounds like conjecture at this point) How would that be evidence for Common Descent? It says nothing about specific phylogenetic branching patterns, (by definition Orphan Genes lack that information) only that two species that are less similar to each other already, will be less similar in another way.

    And to make a more general point, you (like all evolutionists) are appealing to non-existent mythical fairy-tale transitional creatures to fill those genetic gaps.

    If someone like Nelson or Sal, who are trying to make something out orphan genes…

    It isn’t just evo critics making something of orphans. Honest evolutionists are genuinely mystified by their existence. Here’s one example:

    Ken Weiss – Professor of Biological Anthropology & Genetics PSU

    “How Can There Be Orphan Genes?” May 2012
    http://molecularevolutionforum.....genes.html

    The basic story up until now has been that molecular evolution is a very gradual process, involving successive modifications upon existing genetic function, leaving a long trail genetic homology. The emerging pattern of widespread de novo function of orphans turns that idea on its head.

    This seems to be a strange, but well-known phenomena with evolution: where a major discovery defies all predictions of the theory, but is almost instantly assimilated and becomes more evidence for the theory. Orphans have already become evidence for the power of random processes to strike on novel function. Evolution is like some kind of invincible horror-movie Blob monster with the way it handles data.

  26. 26

    If, per some enigmatic reasoning, the presence of orphan genes is evidence in favor of common descent via gradual transitions, then how, pray tell, would their absence count as evidence against it?

    “Even if this turns out to be true (and it pretty much sounds like conjecture at this point) How would that be evidence for Common Descent? It says nothing about specific phylogenetic branching patterns, (by definition Orphan Genes lack that information) only that two species that are less similar to each other already, will be less similar in another way.”

    Well said.

  27. Lifespy, you aren’t getting it.

    Is Fig 1. http://gbe.oxfordjournals.org/...../439.short a speculation? Of course the sequence of orphans themselves don’t provide evidence for common descent. The point I am is that the distribution or “orphan” genes follows a phylogenetic pattern, which is to say most of them are not, in fact, species-specific genes. Just genes for which homologs from other species have not yet been sequenced.

    The fact sequencing the close-relatives of a given species whittles away the number of apparent orphans is absolutely evidence for common descent.

  28. Chance Ratcliff.

    Try and read the posts again. It’s not hte presence of orphans that I”m talking about. It’s the pattern to the number of orphans per genome, and, by extension the shared “lineage-specific” genes that are restricted to phylogenetic groups.

  29. wd400,

    Is Fig 1. http://gbe.oxfordjournals.org/…../439.short a speculation? Of course the sequence of orphans themselves don’t provide evidence for common descent. The point I am is that the distribution or “orphan” genes follows a phylogenetic pattern, which is to say most of them are not, in fact, species-specific genes. Just genes for which homologs from other species have not yet been sequenced.

    The pattern is broken in that study.

    “Most ant genomes contain the expected number of orphan genes given their phylogenetic age. However, three insect genomes significantly deviate from the expected SSOG counts: Genomes of the two leaf-cutter species, appear to be enriched for SSOGs(species specific orphan genes), and the genome of the mosquito Anopheles gambiae appears to be depleted of SSOGs. Even if normalized for differences in evolutionary distances, we found that hymenopteran genomes contain more SSOGs and TSOGs(taxon-specific orphan genes) in comparison with dipterans.”

    What’s the difference? If the pattern holds, Evolution did it. If it deviates, then Evolution did that, too. Your claim that most SSOG’s are just undiscovered homologs is conjecture at this point.

    The fact sequencing the close-relatives of a given species whittles away the number of apparent orphans is absolutely evidence for common descent.

    No more evidence than for common design. Who would argue that if you’re looking for a genetic similarity to an Ant, the most likely place you’ll find it is another Ant? (or a creature with a body plan very much like an Ant, instead of something like a fish or a bird)

    Even if orphan genes are relegated to larger taxonomic groupings, you’re still left with a significant portion of protein-coding function that is essentially appearing randomly out of nowhere in between phylogenetic branchings and mythological speciation events.

  30. you’re still left with a significant portion of protein-coding function that is essentially appearing randomly out of nowhere in

    Have you read any of these papers? Very few of the apparent “orphans” have an entirely unexplained origin. Many have arisen by gene duplication and subsequent rapid evolution (i.e. an “orphan” is homologous to another gene within the host’s genome, which in turn shows homology to other species’ genes), others would be homologous if translated in another frame (so may have arisen by frameshifting mutations), a large proportion are homologous to intergenic DNA.

    In most cases, when people look closely only about ~20% of the orphans have no known origin.

  31. wd400

    Have you read any of these papers? Very few of the apparent “orphans” have an entirely unexplained origin. Many have arisen by gene duplication and subsequent rapid evolution (i.e. an “orphan” is homologous to another gene within the host’s genome, which in turn shows homology to other species’ genes)

    Did you read the paper? Your summary appears inaccurate.

    from “Mechanisms and Dynamics of Orphan Gene Emergence in Insect Genomes” http://gbe.oxfordjournals.org/content/5/2/439.full

    only 10% found paralogs -> homologs

    We identified 1,195 (species-specific orphan genes) SSOGs (9.9%) in the seven ant genomes with detectable sequence similarity to a paralog, that is, another gene in the same species and where this paralog has in turn detectable homologs in other species.

    others would be homologous if translated in another frame (so may have arisen by frameshifting mutations)

    only 2% were thought to be from a frameshift

    Across all seven ant genomes, we identified 268 SSOGs (2.2%) that are candidates for frame shift mutations.

    a large proportion are homologous to intergenic DNA.

    We found significant scaffold matches for 5,239 (43.5%) SSOGs in at least one other hymenopteran species. Among the now six scenarios of origin we considered, this approach identified the largest proportion of SSOGs…

    Overall, we expect that most of the SSOGs with intergenic matches derive from de novo formation or generalized gene loss…

    We have investigated in detail through which mechanisms ant orphan genes were formed. Our results indicate that contrary to the long-standing assumption that new genes originate primarily from gene duplications (Ohno 1970; Long et al. 2003; Zhou et al. 2008), the majority of orphan genes in ants resulted from either de novo formation or generalized gene loss
    —————

    In most cases, when people look closely only about ~20% of the orphans have no known origin.

    Do you realize that “de novo formation” is being used by the researchers as a primary “known origin” of the gene sequences?

    And that’s the whole point of this post and my comments. By assuming evolution is true, evolutionists are forced to accept the widespread and sudden, selection-free origin of novel, functional genetic sequences. It is totally unexpected and totally contrary to the neo-darwinian theory that has been bandied around as a fact for decades.

  32. I did read the paper, and I also know what the authors mean by de novo. They mean an existing intergenic sequence got a cis regulatory element and started making transcripts. That’s not an origin out of nowhere. (I’m also dubious that all these genes annotated by transcripts or ORF-finding programs are actually making functional protein products – the more we have focused on these genes in very well annotated genomes like human the less of them have stood up, but that’s really an aside.)

    As for being “totally unexpected”. I don’t know. Everytime and new “basal” animal genome is sequenced there is a press release (dutifully picked up by creationists) saying how surprising it is that most of our genes have a homolog in this relatively simple animal. Is that expected? The question of gene origins, and the relative important of new genes v new regulatory elements is interesting, but not earth shattering. It’s also certainly nothing like the OP or Nelson seem to think it is.

  33. wd400

    I did read the paper, and I also know what the authors mean by de novo. They mean an existing intergenic sequence got a cis regulatory element and started making transcripts. That’s not an origin out of nowhere.

    It’s not the DNA molecules themselves that are ‘out of nowhere’ but the new function. Like Mung said on a different thread:

    It never ceases to amaze me how we can be told over and over that evolution isn’t a random process, but when you really need to explain something difficult, neutral evolution, and drift, and “it just happened – that’s all” are taken seriously.

  34. right… but if the cousins of these potentially functional genes are sitting in other genomes for us to see that’s pretty strong evidence for how these genes arise, isn’t it?

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