October 7, 2010 | David F. Coppedge

More DNA Repair Wonders Found

One of the most phenomenal discoveries since the structure of DNA was revealed must surely be the discovery of multitudes of protein machines that repair DNA (01/04/2002).  The repair machines are themselves coded by DNA, but DNA would quickly decay into nonsense without them.  Another “fundamentally new” repair mechanism was discovered by researchers at Vanderbilt University recently, and other scientists reporting in Nature uncovered more secrets of a “key player” in DNA double-stranded break repair.
    Science Daily began its echo of the university press release saying, “Tucked within its double-helix structure, DNA contains the chemical blueprint that guides all the processes that take place within the cell and are essential for life.  Therefore, repairing damage and maintaining the integrity of its DNA is one of the cell’s highest priorities.”  The wording brings to mind a well-managed business.  How can a cell have priorities, integrity, and maintenance?
    Explaining that DNA is highly reactive, the article goes on to describe how DNA damage repair is a constant process.  “On a good day about one million bases in the DNA in a human cell are damaged.”  That’s on a good day.  Toxins, reactive oxygen, radiation, and just normal chemical activity in the cell can lead to all kinds of problems.  Untreated, these damages can lead to cell death or cancer.  The newly discovered mechanism acts on DNA bases that become alkylated.  This results in “lesions” on the double helix that can impair translation or replication.  “To make matters worse, there are dozens of different types of alkylated DNA bases, each of which has a different effect on replication.”
    Several known mechanisms can treat the lesions by scanning the DNA chain, something like crewmen on a railroad car, looking for damaged cross-beams, latching onto them and then flipping each one outward and holding it in a special pocket so that other repairmen can attach to the site, fix it, and put it back.  The new mechanism found by the Vanderbilt team operates in bacteria.  It finds the lesion and, unlike most known glycosylases, flips out both the damaged base and the base it is paired with.  Why?  “This appears to work because the enzyme only operates on deformed bases that have picked up an excess positive charge, making these bases very unstable,” the article explained.  If left alone, the deformed base will detach spontaneously.”  This specialized enzyme may attract other repair enzymes to the site, and “speeds up the process by about 100 times.”  The enzyme “uses several rod-like helical structures … to grab hold of DNA.”
    What’s more, this enzyme is “considerably different from that of other known DNA-binding proteins or enzymes,” though it bears some resemblance to a family of “very large molecules that possess a small active site that plays a role in regulating the cells’ response to DNA damage.”  The article said nothing about evolution.
    On another DNA-repair front, today’s Nature described a “protein giant” named BRCA2 that is critically involved in DNA repair, specifically targeting the dangerous double-stranded breaks that can lead to serious health consequences (double-stranded breaks, as the name implies, involve both rungs of the DNA ladder separating).  The BRCA2 enzyme, more than 400 kilodaltons in size (containing roughly 400,000 atomic mass units), is a “key player” in the repair, said Lee Zou [Harvard] in Nature,1 commenting on a paper by Jensen et al in the same issue that elucidated the structure of this giant fix-it molecule and explained how it works.2  Since it repairs damage that can lead to breast and ovarian cancers and Fanconi anemia, BRCA2 is of great interest to medical researchers and their patients.  Zou described and illustrated four specific functions of this enzyme in the multi-player teamwork process that fixes double-stranded breaks.  In addition, the “histone code” (07/26/2006) appears to play a role in regulating the whole repair team.  Both articles mentioned evolution only in passing, suggesting possible ancestral relationships, but only in a most cursory and ancillary manner.

1.  Lee Zou, “DNA repair: A protein giant in its entirety,” Nature 467, pp. 667?668, 07 October 2010, doi:10.1038/467667a.
2.  Jensen, Carreira and Kowalczykowski, “Purified human BRCA2 stimulates RAD51-mediated recombination,” Nature 467, pp. 678?683, 07 October 2010, doi:10.1038/nature09399.

How Darwinism can survive in today’s environment is a tale of the capacity for humans to cling to dogma far beyond whatever usefulness it may have had.  Darwinism may have made 19th-century Victorian racists in the British empire feel like they had latched onto something.  It may have allowed certain racist totalitarian tyrants to justify their atrocities with a veneer of scientific credibility.  That was all before 1951, when the basis of heredity was found to involve a coded language.  Shortly after, Crick discovered that one code gets translated by a family of interpreters into another code.  Now, in the 21st century, we have whole systems of molecular machines dedicated to preserving the code, and codes upon codes regulating the codes.
    Darwin didn’t write code.  Software was only beginning to be invented by Babbage in those days.  Darwin knew nothing about networks and codes and double-stranded breaks with BRCA2 machinery at the ready, and other complex mechanisms operating even in bacteria, the simplest little blobs of protoplasm he envisioned, that turned out to be more complex than any machinery in Britain.  Why must we cling to an outmoded view of life that spun from minds eager to rid science of intelligent causes?  We need a biology for the Information Age, where intelligent causes are well known.  Intelligence, and only intelligence, explains codes, messages, software, error-correction routines, networks, and hierarchical systems of all the above.  Step aside, Charlie.  You had your day.  You did your damage.  We have a lot of repair work to do.

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