Intelligent Design

Fact-Checking Wikipedia on Common Descent: The Evidence from Observed Natural Selection

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A few weeks ago, I published the fourth part of my series on Wikipedia and common descent, in which I discussed the purported evidence for common ancestry based on biogeographical distribution. Previously, I had cross-examined the evidence from comparative physiology and biochemistry, comparative anatomy, and paleontology. In this second-to-last installment, I will address Wikipedia’s evidence from observed natural selection and speciation.

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13 Replies to “Fact-Checking Wikipedia on Common Descent: The Evidence from Observed Natural Selection

  1. 1
    Scootle says:

    Negoro et al (2005) on the Nylon-degrading enzyme:

    6-Aminohexanoate-dimer hydrolase (EII), responsible for the degradation of nylon-6 industry by-products, and its analogous enzyme (EII´) that has only ~0.5% of the specific activity toward the 6-aminohexanoate-linear dimer, are encoded on plasmid pOAD2 of Arthrobacter sp. (formerly Flavobacterium sp.) KI72.

    We have found that of the 46 amino acid alterations that differed between the EII and EII´ proteins, two amino acid replacements in the EII´ protein (i.e. Gly to Asp (EII-type) at position 181 (G181D) and His to Asn (EII-type) at position 266 (H266N)) are sufficient to increase the Ald-hydrolytic activity back to the level of the parental EII enzyme. The other 44 amino acid alterations have no significant effect on the increase of the activity.

    [IMAGE]

    The activity of the EII´-type enzyme is enhanced ~10-fold by the G181D substitution and ~200-fold by the G181D/H266N double substitutions. Nylon oligomer hydrolase utilizes Ser112/Lys115/Tyr215 as common active sites, both for Ald-hydrolytic and esterolytic activity, but requires at least two additional amino acid residues (Asp181/Asn266), specific for Ald-hydrolytic activity.

    These results indicate that the G181D and H266N are amino acid alterations specific for the increase of nylon oligomer hydrolysis. Thus, the nylon oligomer-degrading enzyme (EII) is considered to have evolved from preexisting esterases with ?-lactamase folds.

  2. 2
    Collin says:

    Jonathan,

    It seems like you admit that these are examples of the creation of information by evolution.

  3. 3
    Jonathan M says:

    Collin,

    Sorry I’m not sure how you get that idea from what I wrote. Please elaborate. Thanks.

    J

  4. 4
    bornagain77 says:

    OT:

    What Do Organisms Mean? Stephen L. Talbott
    Editor’s Note: This is the third in a set of essays by Mr. Talbott dealing with the new understanding of living organisms being urged upon us by the intense ongoing work in molecular biology. The previous installments were “Getting Over the Code Delusion” (Summer 2010) and “The Unbearable Wholeness of Beings” (Fall 2010).
    http://www.thenewatlantis.com/.....nisms-mean

  5. 5
    Geoxus says:

    “Natural selection is tantamount to common descent”? Excuse me if I don’t follow the logical progression. Common descent does not logically entail natural selection as the evolutionary mechanism, nor does the occurrence of natural selection entail the validity of common descent. I would have thought this to be fairly basic.

    Good, you found a true and important flaw in the article (it was about time!). Common ancestry is a pattern. NS is a process that can explain some of that pattern. NS helps to show that linage bifurcation is possible, but this is not evidence for CA by itself. I’d remove the whole section.

    I would have thought this to be fairly basic. Evidently not.

    It is.

    But this phenomenon can hardly be construed as genetic novelty. Indeed, this adaptation is accomplished by a loss of genetic information. The “novel” ability is acquired by a mutation that shuts off the capacity for production of the enzyme lactase.

    The novel feature is the lactase production beyond early childhood. The mutation prevents lactase production from being shut off.

    […]Not even the most rock-ribbed young earth fundamentalist creationists[…]

    Hey, that’s not nice. Never offend a costumer.

  6. 6
    bornagain77 says:

    Excerpted quotes from preceding article

    What Do Organisms Mean? Stephen L. Talbott – Winter 2011
    Excerpt: Harvard biologist Richard Lewontin once described how you can excise the developing limb bud from an amphibian embryo, shake the cells loose from each other, allow them to reaggregate into a random lump, and then replace the lump in the embryo. A normal leg develops. Somehow the form of the limb as a whole is the ruling factor, redefining the parts according to the larger pattern. Lewontin went on to remark: “Unlike a machine whose totality is created by the juxtaposition of bits and pieces with different functions and properties, the bits and pieces of a developing organism seem to come into existence as a consequence of their spatial position at critical moments in the embryo’s development. Such an object is less like a machine than it is like a language whose elements … take unique meaning from their context.[3]”,,,

    ,,,But we now know from the vast literature on gene regulation (oddly, Sean Carroll does not even mention epigenetics in his book) that those supposed switching networks are in fact penetrated and influenced by virtually everything going on in the cell. ,,,(Sean) Carroll repeatedly talks about how various genes “sculpt” a fly’s wings and various anatomical structures of other animals, adding that the action of these genes “in organizing, subdividing, and specifying and sculpting parts of the embryo becomes clear when visualized.” But it’s obvious enough that a section of a DNA molecule does not “sculpt” anything. In fact, the research emphasis today is in the reverse direction: how proteins and the overall activity of the cell sculpt the genes and chromosomes. ,,, The activity of individual genes reflects the choreography of chromosomes, which reflects the larger choreography of the nucleus, which reflects the choreography of the cell and organism as a whole. Who, then, is sculpting whom?,,,
    http://www.thenewatlantis.com/.....nisms-mean

  7. 7
    Starbuck says:

    The mechanism of resistance is mutations affecting this enzyme. And there are many different modifications that can be made, which result in the acquisition of resistance to sulfonamides. This suggests that merely a modification of a target site is involved in conferring resistance.

    No. (it can be but usually isn’t) In most cases, resistance is caused by novel genes that are already sulphonamide insensitive e.g. sul2, and these genes come from elsewhere. The bacterium retains its sensitive enzyme.

    Nor does resistance come without a cost. Indeed, there is a tradeoff between resistance to sulfonamides and the performance of the dihydropteroate synthetase enzyme. The mutant bacteria thus incur a fitness cost as compared to the wild type. In order to overcome this decrease in fitness, compensating mutations are acquired in some instances.

    Maybe with mutants there’s a cost – it’s not true for acquired genes, where there is absolutely no evidence of a cost, but many claims that there is one. Many people in this field talk a lot of rubbish, all very confused and unsubstantiated.

    With regard to vancomycin resistance, the first paragraph of your is correct, but the 2nd paragraph is dealing with full blown vancomycin resistance due to acquisition of the vanA operon. Vancomycin is a glycopeptide that interferes with the production of peptidoglycans. It does this by virtue of binding to the carboxyl terminus of peptidoglycan stem peptides, thus blocking the cross-linking of peptidoglycans.

    While high level vancomycin resistance in S. aureus is due to the acquisition of the VanA operon from enterococci, the mechanisms of intermediate level vancomycin resistance have been less well defined. Intermediate vancomycin resistance in clinical S. aureus can be generated by single base substitutions in key staphylococcal regulatory genes. Not only can a single base substitution confer intermediate vancomycin resistance, but can also cause cross resistance to another important antibiotic, daptomycin.

  8. 8
    Starbuck says:

    Regarding the sentence “Thus, the critical mechanism of resistance is the synthesis of D-Ala-D-Ala, which has the capacity for ester formation.”, did you mean to state
    D-Ala-D-lactate?

  9. 9
    Starbuck says:

    With regard to Nylon eating bacteria, structural analysis of Hyb-24 reveals the structural similarity to beta-lactamase-folded proteins. The following paper strengthens the hypothesis that the nylon oligomer hydrolase (EII) evolved by gene duplication from the common antecedent of EII and cryptic EII’ proteins located on the same plasmid.

    Negoro et al (2007). Nylon-oligomer degrading enzyme/substrate complex: catalytic mechanism of 6-aminohexanoate-dimer hydrolase. J. Mol. Biol., 370, 142-156.

  10. 10
    Jonathan M says:

    Yes. Thanks for highlighting that typo. It’s now fixed.

    J

  11. 11
    Jonathan M says:

    Starbuck: Please check out this paper – http://www.sciencedirect.com/s.....4600901468

    Regarding fitness cost, the paper states,

    As mentioned above, laboratory mutants in folP show a trade-off between drug resistance and DHPS enzyme performance as reflected in an increased Km for the normal PABA substrate. It could then be surmised that clinically occurring resistance mutants would be at a disadvantage in the absence of sulfonamide, be selected against, and disappear. The examples mentioned above, regarding S.pyogenes and N. meningitidis, show that this will not happen. In the latter case this was explained by the resistant strains acquiring mutations compensating for the disabling effects of resistance changes. The sulfonamide resistance seen today in N.meningitidis could thus be regarded as a scar left from the earlier intensive use of this drug for treatment and prophylaxis of meningococcal disease.

  12. 12
    Mytheos says:

    Fact checking?

    Kind of an oxymoron.

    Shows how sad the state of the world really is.

  13. 13
    MrDunsapy says:

    Though ‘evolution’ is impossible, as proven by the evidence, and reason.
    You are not totally out to lunch either. But it is more like many common ancestors. So uncommon decent is not totally correct either, but getting close. There are definite patterns, that can not be ignored.

    I have an article on this if the people here will let me post it? And I will respond to the questions or answers I get.

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