Intelligent Design

Ultraconserved Phenotype

Spread the love

Between 160 and 240 million years of cumulative divergence between two tiny worms resulted in the genomic divergence by sequence comparison you’d expect over that time yet virtually no phenotype divergence. Once you’re a nemotode you’re always a nematode? Who would have predicted that…

Caenorhabditis comparative genomics [18 November 2003]

Analysis of the sequence revealed that major evolutionary changes in genomes do not necessarily lead to gross physical changes in the adapted organism. “C. elegans and C. briggsae diverged 80 to 120 million years ago, somewhat longer ago than human and mouse,” Stein wrote in an E-mail to us. “By several measures, the two nematode genomes are very much scrambled relative to each other – far more than human and mouse are. Yet while human and mouse are extremely different in ecological niche, behavior, and anatomy, the two nematode species occupy identical niches, have similar behavior, and are indistinguishable except to experts.

Google ultraconserved phenotype for more information.

20 Replies to “Ultraconserved Phenotype

  1. 1
    RobertC says:

    DaveScot,
    The article suggests that ” “the difference is almost entirely due to repetitive sequences, which accounts for 22.4% of the C. briggsae genome in contrast to 16.5% of the C. elegans genome.” Arrangements of operons were highly conserved, with the greatest divergence observed in the chromosomal arms as opposed to the centers.”

    So the genome has ‘scrambled’ over time, but a lot of genes are actually conserved. From the article, it seems like they are suggesting that gross rearrangements don’t necessarily yield new phenotypes in two organisms occupying the same niche.

    So I get the Darwinist rational from the article.

    What would you suggest the intellegent design counter hypothesis is?

    I guess “they’ve been designed as worms” so they resist change might be one.

  2. 2
    DaveScot says:

    Nematode trivia: 20,000 coding genes

    Further quote from same article:

    Avril Coghlan at Trinity College Dublin told us, “What was astounding about the C. briggsae-C. elegans comparison is that of all the conserved regions that could be found between the two species, only one third lie inside coding regions of genes.

    Astounding, unexpected, surprising… is there a theme emerging here from comparative genomics about how well NDE predictions are holding up as the gene bank gets bigger?

  3. 3
    littlejon says:

    I don’t quite understand this response. Did not Robert C specifically ask about the “intelligent design counter hypothesis”? Am I missing something – how is “how well NDE predictions are holding up” relevant?

  4. 4
    Michaels7 says:

    Dave,

    You guys need to see the Ad in American Society for Cell Biology newsletter.

    “â–  Join the ASCB Public Policy Advocacy Team
    â–  Are you interested in public policy advocacy?
    â–  Concerned about federal funding for biomedical research in America?
    ■ Worried about intelligent design being taught in America’s science classrooms?*
    â–  Interested in educating your elected representatives about the importance of biomedical research?”

    *bold my emphasis, its a 50 state push.

    Appears in Volume 29, No. 12, 12/01/2006, page 19 of 44. A PDF file: http://www.ascb.org/filetracker.cfm?fileid=552

    or link http://www.ascb.org/index.cfm?navid=75 and click on December 2006 newsletter.

    So, ID will ruin Cell Biology in the future. ooooh boogey man ID!

    Reading the President’s column on her experience as an “undergrad” and grad student is rather enlightening as well in relation to “central dogma.”

    You can delete this comment, but wanted to notify ya, if interested.

  5. 5
    Michaels7 says:

    littlejon,

    Dave’s comment was posted prior to RobertC.

  6. 6
    waldteufel says:

    So . . . .exactly how does the referenced article advance ID? I haven’t seen any comments regarding how the ID concept is furthered here.

  7. 7
    Jehu says:

    Robert C,

    So the genome has ’scrambled’ over time, but a lot of genes are actually conserved. From the article, it seems like they are suggesting that gross rearrangements don’t necessarily yield new phenotypes in two organisms occupying the same niche

    Duh. The nemotodes are genetically less similar than human and mouse, yet they look the same. That is a suprise and it is very interesting. It may be that the nematode is a molecular monument neutral drift or it may be something else.

  8. 8
    tribune7 says:

    From the article, it seems like they are suggesting that gross rearrangements don’t necessarily yield new phenotypes in two organisms occupying the same niche. . .So I get the Darwinist rational from the article.

    So do I.

    If it happens Darwin predicted it.

    If it doesn’t happen, Darwin predicted it. 🙂

    What would you suggest the intellegent design counter hypothesis is?

    You have a simple observation that worms remain worms despite significant changes in the genotype. Now you want to know why worms remain worms rejecting out of hand the possibility they were designed that way. Why?

  9. 9
    gpuccio says:

    RobertC,

    I think the ID counter argument (more than “hypothesis”) could be:
    1) We really (and I mena really!) have no idea of where is the information which makes a worm a worm, and a human a human.
    2) Nothing in the accumulating data from genomes supports the traditional view that the relevant information is in the genes which code for proteins.
    3) Wherever that information is (non coding DNA, unknown strata of code in DNA or in other biological structures,… ?), it works, it is higly efficient, it is higly structured.
    4) As far as we know, such a “dark information” (just using the term in analogy to dark matter and dark energy, but I think it could be funny to name it this way…) could very likely support the ID point of view, while it seems very unlikely that it will be of help to our darwinian friends. You may ask why, but I know that deep in the heart you agree, so I won’t spend more words on that. Time will say.

  10. 10
    DaveScot says:

    The ID front loading hypothesis predicts that the information required to build novel cell types, tissue types, organs, and body plans is present before they are expressed. The major objection to this is that random mutation will destroy the information absent selection pressure over deep time.

    In this odd case we have genomic information that has been subject to random mutation for 200my between two lines resulting in major changes in the genome yet the information, or plan if you will, for building this particular nematode has been ultraconserved despite 200my years of random mutation in two different species. Any instances where deep time conservation has ocurred when random mutation should have caused a divergence is evidence in support of mechanisms that can conserve information that shouldn’t have been conserved under the rm+ns paradigm.

  11. 11
    pegase says:

    @ DaveScot: “…has been ultraconserved despite 200my years of random mutation [and natural selection] in two different species…

    That sounds better this way; but then this isn’t helpful for ID, isn’t it?

    You seem to forget half of the framework each time you are discussing biology.

  12. 12
    DaveScot says:

    pegase

    When half the framework is rendered inoperative by the other half it’s noteworthy. No phenotype evolution took place here despite 250my of “evolution” which operated in normal fashion on the genotype. The NDE prediction is that phenotype variation is largely due to genotype variation. I suggest you read the wiki page on phenotype again. Pay particular attention to:

    “Phenotype is determined to a large extent by genotype”

    “Phenotypic variation (due to underlying heritable genetic variation) is a fundamental prerequisite for evolution by natural selection.”

    “genotype + environment + random-variation → phenotype”

    In this case it was “environment → phenotype”. Random mutation varying the genotype had no phenotype effect for 250 million years!

    P.S. If you’re going to quote me don’t change it or insert extra things into it. Consider yourself warned.

  13. 13
    Chris Hyland says:

    “1) We really (and I mena really!) have no idea of where is the information which makes a worm a worm, and a human a human.”

    We don’t know what causes every difference obviously but we have a fairly good idea of what makes a worm a worm, its a very well studied organism especially it’s development.

    “Nothing in the accumulating data from genomes supports the traditional view that the relevant information is in the genes which code for proteins.”

    Some of it is. A lot of it is in the regions that control the expression of genes. There probably are some important noncoding genomic elements that we are not currently aware of but Im not sure how this helps ID.

    I think the point here is genomic change is (usually) necessary for does does nor guarantee phenotypic change, especially as the two species occupy the same niche.

  14. 14
    jimbo says:

    This seems more proof of Rupert Sheldrake’s hypothesis that biological form is a field effect, not determined by any form of “genetic program”. ..

  15. 15
    gpuccio says:

    Chris Hyland:

    “We don’t know what causes every difference obviously but we have a fairly good idea of what makes a worm a worm, its a very well studied organism especially it’s development”

    I don’t agree that we have a fairly good idea of anything like that. The only clue that we have about morphologic arrangement in multicellular organism, for instance, is the small knowledge about homeobox genes, which in my opinion is vastly overrated (homeobox genes are obviously important terminal genes for the process, but there is no reason to think that they control the process itself). We know nothing about the control of cell differentiation, of gene expression, of neuronal connections, of tissue specificity, and so on, just to mention a few problems in multicellular organisms. In other words, we know something about a few effectors (the proteins), but we know nothing about the procedures, that is the true program, the true code. The fact that nematodes and men share the same number (approximately) of genes, and that many of them are similar, should truly be a reason of worry for darwinians. What is that makes the difference? What information gives form and structure, for instance, to the human central nervous system? What do we know of all that? Nothing at all!
    We have no idea of where the code for the procedures is, that’s the simple truth, and the fact that humans and nematodes may have similarities far beyond expectations (almost the same number of genes!), that two almost identical nematodes may show great divergence in great part of teir genome without any phenotipic correspondence, and many other data which are accumulating, are great problems for the traditional scenario.
    Everybody now agrees that the central dogma “one gene one protein” was a great mistake and is not true. So biologists say: one gene, many proteins, and they think they have given an answer to something. But what kind of an answer is that? Who tells the single gene which of the many possible proteins should be produced in any particular circumstance? Again, where is the code, where are the procedures, where is the control?

    “There probably are some important noncoding genomic elements that we are not currently aware of but Im not sure how this helps ID”

    That is really an understatement! We still believe that we understand most of genetic information! The truth is that the about 10 Mbytes of the protein coding genome cannot in any way explain the complexity of the human organism (or, for that, of any simpler multicellular organism). The problem is that darwinian evolution can be already proved false if we reason about the complexity of the protein coding genome (see Behe, Dembski, and all the ID scenario: they are absolutely right, as anybody with some sense should understand). But just try to imagine how much more unlikely darwinian evolution will be when we discover that the development of single cells and of macroscopic structures is controlled by a much more complex code, maybe of Gigabytes of information, or more, a code that presently we have no idea of, which is completely missing to our present understanding. A code which controls DNA spacial structure, its ordered and differentiated transcription, all the post-transcriptional maturations, and which is responsible of the balance, error control, specificity, of each single cell and of the complex interrelations of billions and billions of different cells at each moment. When we discover something about that code, about the procedures and the control, then I doubt that anybody will still have the courage to think that all that was spontaneously developed by means of random mutation and natural selection…
    So, yes, the constant disclosure of new levels of complexity does help ID, it helps ID a lot, and that’s the reason why ID is spreading now, and not 50 years ago! Each new contradictory data, each new mystery we find in our understanding of the genome or of biology, is a precious occasion to develop new perspectives and to deliver ourselves from the unlikely lies which have usurped the scientific field in the last few decades.

  16. 16
    DaveScot says:

    gpuccio – well said!

    I know what makes a worm a worm though. A momma worm!

  17. 17
    Michaels7 says:

    I think reading the Presidents column in ASCB newsletter is helpful along the lines of what we know/don’t know then and now.

    Current President, Mary Beckerle comments,
    “As an undergraduate, I learned cell biology and I had the distinct impression that the major questions were answered, the major paradigms developed. Still,I loved biology,and I went to graduate school. In one of my earliest classes, I learned that it really wasn ’t clear at all how a critical cell structure —the plasma membrane — was organized.”

    “Shocked” I tell you,
    “I admit to being somewhat shocked since my
    undergraduate textbook had made membrane structure seem so well-established and, in retrospect, so static.
    That ’s it, I thought to myself:
    Understanding the structure of the plasma membrane is the final frontier.”

    This is an intelligent person remembering her experiences as an undergrad. As a student in advanced biology and chemistry in high school and in undergrad courses at university, I too remember thinking similar thoughts, all things known, solved.
    Looking back I realize how much arrogance was oozing through the poors of the materialist professors of “Central Dogma”. This aligns with Gil’s post earlier.

    She continues,
    “During that time, one thing you could always count on was the Central Dogma: DNA to RNA to Protein. Clean and simple. Then along came RNA splicing, editing, and interference, and completely unanticipated, new understanding about the diversity of genetic information.”

    “Completely unanticipated” is honest hindsight, but not one you hear much. Especially among the faithful robot followers of the likes of PZ, etc.

    I think the complexity of information discovered or the manipulation of information within the cell, was undermined since the beginning of the days that evolutionist thought this was random globs coming together. When you think something is unguided, unpurposed, you would not think it to be complex.

    That scientist whether ID or Creationist have and can do this same type of research work in operational genetics and molecular biology, makes their questions and critiques more relevant today, and still yet undervalued.

    She says, “Dream big…”
    ” We must focus on the most important questions,the hard questions that have the possibility of opening new areas of investigation and new ways of thinking. How can we encourage the type of risk-taking that is necessary for the most innovative science? We must dare to be bold. We must demand creativity and change. We must support our
    colleagues who are probing new areas.”

    Right, so she supports the creation of a lobby to oppose ID. Yep, give me that old time Stalinista oppression that sure encourages bold, innovative thinking in science and our youth.

    Complete, utter hypocrisy. Bold/Oppress! Risk/Form a Lobby against new ideas!

    Beckearle talks of taking risk, but refuses to think about the possibility of Design. She’s acting more the part of a politician, not a “creative,” “bold” scientist.

    Failures of the past predictions continue to mount up. Is this being truthfully taught to our children?
    If science is the pursuit of truth, then maybe they should Boldly tell the children about these glaring mistakes. But then that would require honesty and the children might start second-guessing all the mini-gods of evolution.

    Maybe she should rethink what is “risk.” Sticking to old, flailing paradigms or looking at new, bold ideas, like ID, that might provide more insight from an Engineering, CS, Phyics, Math perspective.

    “Creative work at the edge is what has propelled our
    field forward in the past. Continuing to work at the
    edge is essential for discovery and for the future of
    cell biology.”

    Uhuh… as long as it stays within politically correct materialistic paradigms.

    But, at least she gets part of it, without admitting the implications of ID…

    For a cell biologist, a collaboration with a colleague
    in mathematics, engineering, computer science,
    chemistry, physics, or medicine
    could serve as
    a bridge. Interdisciplinary interactions allow the collision of diverse ideas that can spark new ways of thinking about a problem.

    Sure, when you bring in hard sciences, engineers and computer scientist who live, breathe and eat from a Design perspective – it should spark new ideas.

    Agreed! Let the new Design Paradigm reign!

  18. 18
    CJYman says:

    Is it at all possible that this research is relevant to a scientific paper that was published in “Proceedings of the Biological Society of Washington” but later “unpublished” due to its author’s heretical non-NDE views?
    http://www.discovery.org/scrip.....38;id=2177

    In line with post 15:
    Furthermore, if this involved even deeper “uber-codes,” wouldn’t they even be more susceptible to harmful mutations: ie – if the smallest amount of information at this level were “mutated” then there could easily be a chain effect which could be devastating; as in multiple proteins, functions, and “location codes” being damaged at once thus rendering the organism good as toast.

  19. 19
    PaV says:

    Mendel came along, and they said (a la Bateson), where did these genes come from.

    Fisher, Haldane, and Sewell Wright came along and said random changes can make these genes appear.

    Then the Central Dogma implying that random molecular changes (SNP’s, if you will) can explain it all.

    But then experiments like this one and Rubin’s come along, which, together, completely destroy any connection between phenotype and genotype; thus destroying the Modern Synthesis.

    Now in the latest Nature, we hear that they’ve found that there is a ‘code within a code’ in DNA that utilizes the “degeneracy” of DNA code to superimpose another code atop the primary code. This now deals a death blow to the Neutral Theory.

    So, what’s left? Evo-devo; that’s it. The problem is: evo-devo might tell you the ‘recipe’ for making cells, but it gives no clue as to how the ‘ingredients’ came about. But apparently nothing has the power to kill this incoherent theory. It’s like a feline science: it has nine lives! Get out the garlic wreath…….!#%!

  20. 20

    […] Natural selection can work so well that ~120 million years of random mutation on two different species of worm, with genomes comparatively scrambled moreso than man and mouse (~90my), somehow retained virtually identical phenotypes. […]

Leave a Reply