February 13, 2004 | David F. Coppedge

“Utmost Precision” Found in DNA Repair Enzyme

The cell has many helper enzymes that can repair DNA damage.  One such enzyme, named MutY, has been described in the Feb. 12 issue of Nature.1  Reviewer Tomas Lindahl sets the stage: “Damaged DNA must be removed with the utmost precision, as mistakes are costly.  The structure of a repair enzyme bound to its substrate provides a welcome clue to how this is achieved.”
    This particular enzyme is able to recognize its particular error target, an adenine incorrectly paired to an oxidized guanine, because of “extensive and precise contacts” it makes with that specific erroneous pair.  These contacts prevent it from mistakenly removing a correct pair.  In a paper in the same issue, Fromme et al.2 describe “an ingenious way by which this specificity is achieved” through these multiple, precise contacts.
    Lindahl describes how this enzyme works.  Details of the jargon are not essential for appreciating the precision of this molecular machine’s lifesaving activity:

MutY belongs to a group of enzymes known as DNA glycosylases, which recognize altered bases in DNA and help to remove them.  Like other DNA glycosylases, it generates a sharp bend in the DNA at the site of the mismatch.  The new structural data provide a suitable explanation for why – as is desired – MutY doesn’t recognize and remove an adenine opposite its normal base partner, thymine (T): the extensive and precise contacts between MutY and an A•xoG pair are entirely absent in a normal AT pair.  Similarly, the enzyme’s active site does not accommodate a cytosine opposite an oxoG; for coding reasons, it is important that the oxidized base rather than the normal base is repaired in this partnership.

Lindahl notes that mutations in this enzyme put humans at risk of colorectal cancer.  Other oxygen-altered bases, if not repaired, are implicated in tissue degeneration and ageing.


1Tomas Lindahl, “Molecular Biology: Ensuring error-free DNA repair,” Nature 427, 598 (12 February 2004); doi:10.1038/427598a.
2Fromme et al., Nature Feb 12, 2004, p. 652.

How does a blind molecule do this?  Notice how specific the contacts are: some parts first allow the enzyme to contact the specific error-bound pair, and if and only if a match is found, other parts of this machine are designed to bend the DNA strand so that the bad base can be cut out.  (He didn’t go into this, but other machines are on hand to ferry in and insert the correct base.)  All these extensive and precise contacts exist because another section of DNA that codes for this enzyme contains bases that are also extensive and precise.  This underscores the principle that enzymes, to work, are not indiscriminately mutatable.  They have to be precise to work.
    It also underscores the evolutionary conundrum that DNA needs repair enzymes to prevent catastrophic errors, but the repair enzymes themselves are coded by DNA.  How could a DNA strand without the error-correction mechanisms survive beyond a few copies?  Evolutionists know that accurate copying is essential to prevent “error catastrophe” yet they expect us to believe that these marvelous high-precision error-correction systems (and there are many, many parts of the DNA Damage Repair team), somehow came into being via accidents.  Give me a break.  (On second thought, don’t–broken DNA is deadly.)  Not surprising that there is no mention at all of evolution in this article.
    For more on the wonder of enzymes and their precision, see our online book, Evolution: Possible or Impossible?  Though written years ago, the book’s thesis that chance is utterly incapable of producing such incredible precision of function is only amplified by discoveries like this.

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