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Human DNA repair process video – by chance?

More details of DNA repair have been revealed.
See: Human DNA repair process recorded in action (Video)

(PhysOrg.com) — A key phase in the repair process of damaged human DNA has been observed and visually recorded by a team of researchers at the University of California, Davis. The recordings provide new information about the role played by a protein known as Rad51, which is linked to breast cancer, in this complex and critical process.
. . . In 2006, the researchers recorded a portion of the bacterial DNA repair process, a system considerably less complex than its human counterpart.. . .

This filament composed of a fluorescently-labeled DNA molecule and the repair protein Rad51 grows progressively brighter and longer as more and more Rad51 molecules assemble onto the DNA.

Human DNA is under constant assault from harmful agents such as ultraviolet sunlight, tobacco smoke and a myriad of chemicals, both natural and man-made. Because damage can lead to cancer, cell death and mutations, an army of proteins and enzymes are mobilized into action whenever it occurs.
. . .
Rad51 takes a leading role in the action. Always on call in the cell, molecules of the protein assemble into a long filament along a damaged or broken segment of DNA, where they help stretch out the coiled strands and align them with corresponding segments on the cell’s second copy of the chromosome, which serves as a template for reconstruction. Because this protein is regulated by a gene linked to increased risk of breast cancer, BRCA2, it is also thought to play a role in suppression of that disease.

With the ability to watch the assembly of individual filaments of Rad51 in real time, Kowalczykowski’s team made a number of discoveries. Among those are that, in contrast to their bacterial counterparts, Rad51 filaments don’t grow indefinitely. This indicates that there is an as-yet undiscovered mechanism that regulates the protein’s growth, Kowalczykowski said.

Another surprising difference between the human and bacterial processes, Kowalczykowski said, is that Rad51 doesn’t fall away from the DNA when repair is complete. Instead, proteins that motor along DNA are required to dislodge it.

See full news item:

Article: Jovencio Hilario, Ichiro Amitani, Ronald J. Baskin, and Stephen C. Kowalczykowski, Direct imaging of human Rad51 nucleoprotein dynamics on individual DNA molecules, PNAS 2009 106:361-368; doi:10.1073/pnaires.0811965106

In review, the steps identified here:
1) Detect DNA damage
2) Call repair mechanism
3) Assemble protein into a long filament
4) Locate it along the damaged/broken segment of DNA
5) Stretch out the coiled strands
6) Align corresponding strands with cell’s second copy of the chromosome
7) Reconstruct using the second chromosome as a template
8) Protein regulated by a gene
9) Undiscovered mechanism that regulates the protein’s growth
10) Motor proteins required to dislodge Rad51 from DNA.

Each of these steps requires highly selective matching configurations. There are probably more steps and regulation involved. This long series of steps suggests an irreducibly complex system.And we are  expected to accept that all this occurred by non-directed random mutations and selection?

How does the organism survive while randomly creating this mechanism? Not having any repair mechanism would probably rapidly lead to death. See Sanford, J. C. 2006. Genetic Entropy and the Mystery of the Genome. Elim Publications. Elim, NY.208 pages.

This evidence looks to me like evidence for blind belief in neoDarwinism!

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12 Responses to Human DNA repair process video – by chance?

  1. Very interesting stuff. If there is anyone out there that has never taken a physiology class, I urge you to pay a little money at a local community college, or maybe take an online course, and witness just how amazing most biological systems are. The human body is a collection of thousands of brilliantly designed sytems all working together

  2. So if evolution happened this would confirm its suicide!(Mutations made complex life and then mutations made an ic mechanism which eliminates mutations to stop further evolution).

  3. Repair requires knowledge

    As in knowledge of what should be and how to fix it.

  4. critiacrof, “mutations made an ic mechanism which eliminates mutations to stop further evolution.”

    If the theory of evolution is correct, this is necessary and positive. The better the repair mechanisms, the more dna can replicate per mutation. There is certainly an upper limit of how many mutations, in functional dna, are possible per organism. Now, I believe, based upon my limited simulations, that the upper limit is one mutation (in functional DNA) per organism. This, is a problem because the average human has at least hundreds.

    It remains however, the tighter the duplication system, the larger the genome that can be supported. I fail to understand how natural selection would “know” this fact, however.

  5. bFast:
    “If the theory of evolution is correct, this is necessary and positive. The better the repair mechanisms, the more dna can replicate per mutation.”
    I see your point. Limiting the mutations is beneficial for the survival and reproduction of the organism. My point is that this mechanism will prevent major changes; with accurate quality control you’ll end up with limited pseudo random variations in stead of lots of random mutations capable of macro evolution. But your point makes this even stronger: this mechanism is essential for live.

    “There is certainly an upper limit of how many mutations, in functional dna, are possible per organism. Now, I believe, based upon my limited simulations, that the upper limit is one mutation (in functional DNA) per organism. This, is a problem because the average human has at least hundreds.”

    Sorry, I lost you at “limited simulations”. Please explain the “problem”.

  6. critiacrof, “I see your point. Limiting the mutations is beneficial for the survival and reproduction of the organism.”

    No, no, my point is not that limiting the mutations is beneficial to the survival of the organism. My point is that the higher the fadelity of replication, the more active DNA an individual organism can have. If an individual organism can withstand a maximum error count, then by reducing the errors, the organism can support more DNA before reaching that maximum — therefore higher fadelity supports greater complexity.

  7. Bfast,very good point with interesting philosophical possibilities. Also you can have great “specificity”- that is even more so than complexity- because specificity has to do with tolerances of a design and such- very specific mechanism obviously cant afford too much stochastic change.

  8. bFast: Ok now I understand. Thank you.
    Still I don’t get this: “Now, I believe, based upon my limited simulations, that the upper limit is one mutation (in functional DNA) per organism. This, is a problem because the average human has at least hundreds.”

    Are you saying that the fidelity allows or should allow only 1 mutation in the DNA? If so I understand the problem. Can you give me some details?

  9. Per critiacrof #5
    Somewhere I have seen a log log graph of mutation rate declining inversely with genome size. (Slope -1). I.e., the larger the genome, the better the replication accuracy and repair to prevent mutations.

  10. 10

    bFast: “…that the uper limit is one mutation … per organism.” etc.

    Two things to consider: the mutation rate can be significantly over 1 if you have sexual reproduction. (I’ve run simulations with stable rates around ~10 per organism).

    And the magnitude of the mutational effect. Empirical studies place the average of one .01 s mutation per organism. (lose ball park) so the rest of the mutation in human DNA have very very slight effects. Of course, if you assume that you can sum an infinite number of very slightly deleterious mutations together (much less than .01), then you would still have a problem. It is obvious that for a sufficiently random sequence mutation pressure will cause just as many slightly beneficial mutation as slightly deleterious ones.

  11. 11

    DLH: Check Drake et. al’s work at http://www.pnas.org/content/88/16/7160.abstract. It is a bit dated, but you’ll find a log log plot in the discussion, and I believe it is the most important empirical paper for most work on the evolution of the mutation rate.

    I’m can’t find a good reference right now, but the trend brakes down for eukaryotes. We don’t have a whole lot of good data, since obtaining genomic mutation rates is hard stuff, but I believe that yeast lay near the regression line, while all other eukaryotes exhibit no clear correlation between genome size and mutation rate (c. elegans, drosophila, h. sapiens)

  12. 12

    For clarification “It is obvious that for a sufficiently random sequence mutation pressure will cause just as many slightly beneficial mutation as slightly deleterious ones.”

    You don’t see mutational meltdown in large populations, even though there are always mutations of sufficiently small effect to escape the action of natural selection.

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