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Speculation on error correction [Re: The fountain of youth.]

Keith Robison robison1 at husc10.harvard.edu
Mon May 11 12:21:28 EST 1992


bradbury at sftwks.UUCP (Robert Bradbury) writes:

>In article <9205081823.AA27075 at rust.zso.dec.com> french at RUST.ZSO.DEC.COM writes:
>>

>I do not believe that gene amplification which normally involves making
>extra DNA to serve as a substrate for transcription is known to occur
>in mammals.  The examples I can think of are Drosophila polytene chromosomes
>or Xenopus oocytes.  If anyone knows of mammalian examples, 
>please enlighten us.

	The only ones I have ever heard about occur in tumor cells under
strong selection.  For example, methotrexate targets dihydrofolate reductase.
In some tumor lines, methotrexate resistance is generated by an enormous
duplication of the DHFR locus.  I believe that a similar mechanism plays
a role in the onset of multi-drug resistance.

>>
>>   * How can you preserve the state of a person's DNA without
>>     also turning off vital functions such as the immune system?
>>

>I'm assuming that you feel that turning on the immune system response
>means destroying the state of the DNA.  This isn't really true.  The
>immune system is designed to be turned on when stimulated by foreign
>substances and will turn itself off when the stimulatory factor is removed.
>Many genes are turned on and off in response to external signals which
>do not involve "destroying" the DNA state.  In fact since "active" DNA
>is preferentially repaired over "inactive" DNA turning genes on is a
>good thing.

	Antibody responses are "matured" by somatic mutations in the 
genes for responding antibodies, coupled with selection for the best
variants (Darwinism on a microscopic scale).  Thus, you might indeed harm
the immune system by shutting down mutation.


>-- 
>Robert Bradbury			uunet!sftwks!bradbury





Keith Robison
Harvard University
Program in Biochemistry, Molecular, Cellular, and Developmental Biology

robison at ribo.harvard.edu 




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