RE: specific amino acid restriction does the same thing as calorie restriction?

From: Robert J. Bradbury (bradbury@aeiveos.com)
Date: Tue Apr 22 2003 - 09:20:40 MDT

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    On Tue, 22 Apr 2003, Rafal Smigrodzki, commenting on Damien's
    comments wrote:

    > nuclear genes, usually present in only two copies, achieve large protein
    > output is by having relatively stable mRNA's which act as amplifiers of
    > their function.

    This may be true -- though I'd like to see some data on what
    regulates the mRNA degradation in eukaryotes. I'm reasonably
    certain that in bacteria (prokaryote) mRNAs are recycled fairly
    rapidly so they can change state more quickly than eukaryotes.

    > If you transfer the mtDNA to the nucleus and set the
    > nuclear-encoded mtRNA polycistronic transcript to a high copy number (by
    > stabilizing it in the cytoplasm), you should be able to make the same amount
    > of protein as made from the 10,000 mtDNAs currently present in our cells.

    Here I'm not so sure -- any context I've seen polycistronic mRNAs
    discussed it is always in prokaryotes. I don't think I've ever
    encountered polycistronic eukaryotic mRNAs. But one can get the
    same effect with multiple gene copies as is the case with the
    ribosomal (rDNA) or transfer (tDNA) genes (which produce (rRNA & tRNA).
    That is common in the larger eukaryotic genomes.

    Polycistronic for those who don't know means that RNA polymerase
    transcribes a single messenger RNA (mRNA) with multiple genes on
    the same RNA strand. It is useful for sets of genes one wants
    to operate in conjunction with each other.

    > I don't know if there is an increase in the mutation rate at highly
    > transcriptionally active loci (where the sense DNA strand indeed has to be
    > pulled open for the RNA to be synthesized), but this couldn't be a higher
    > mutation rate than what you have in the mtDNA now, with all mitos actually
    > recycling their DNA about every two weeks

    At normal body temperatures, if you have two single-strand breaks on
    opposing strands (due to intermediate stages of DNA repair processes
    derived from various types of DNA damage) in a DNA strand at separations
    from 8 to 18 base pairs (depending on the GC:AT composition) then the
    DNA will "melt" producing a double strand break. At fever temperatures
    the separation distance increases slightly. During transcription
    I believe RNA polymerase effectively melts DNA over a larger distance
    still (dozens of base pairs?) so one could get a double strand break
    from single strand breaks located at even larger distances.

    So I would say that yes -- highly transcriptionally active loci would
    be more likely to accumulate mutations since they are more likely
    to incur double strand breaks which produce sequence corruptions
    if they are repaired by the non-homologus end-joining (NHEJ) DNA
    repair pathway.

    [Side note -- this conversation has been quite useful with respect
    to my ideas on a "Grand Unified Theory of Aging".]

    I agree with Rafal that the nuclear mutation rates should be lower
    than the mitochondrial mutation rates. I would expect there ought
    to be data in PubMed on this.

    Robert



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