Bio: Premature Aging; Also, Telomerase (was: Transplants)

Gregory Sullivan (sullivan@oriole.cs.jhu.edu)
Fri, 24 Oct 1997 20:42:25 -0400


Michael Lorrey <retroman@together.net> writes:

> Well, if you look at that aging disease that a few rare kids have, if
> that sort of disorder can be turned on and off in anyone, then you could
> do some sort of rapid development, but I would think that the product of
> such things would tend to be on the short side.

Anders Sandberg <asa@nada.kth.se> said:

>I don't think that works. Progeria makes aging faster, not development
>(otherwise the victims would grow up into adults instead of becoming
>"ancient dwarves").

One rare syndrome that causes "clinical manifestations that resemble
premature aging in humans" is called Werner's syndrome (WS).
Werner's syndrome and progeria are apparently distinct but both cause
premature aging. See:
http://medinfo.wustl.edu/~ysp/MSN/posts/archives/mar97/852909270.Me.r.html

Recently, excellent progress has been made in understanding Werner's
syndrome. See: http://www.bioscience.org/news/scientis/aging1.htm

The Werner's syndrome gene (WRN) has been identified and it is similar
to DNA helicases.

begin excerpt

Helicases are involved in DNA replication, recombination, chromosome
segregation, DNA repair, transcription or any function that requires
unwinding of the DNA. In view of similarity to helicases, the WRN
protein may exert similar functions in cells. Yu et al suggest that
the consequence of the defect in WS patients may be the accumulation
of DNA mutations that ultimately lead to the age-related
manifestations of this disorder. Somatic mutations of oncogenes and
tumor suppressor genes may be the underlying basis for the increased
incidence of cancer seen in these patients. The DNA damage may also be
responsible for premature replicative senescence and consequent
pathologies. Whether the WRN gene is implicated in the normal aging
process remains to be seen, however, the new discovery undoubtedly
will shed light on the pathways that lead to the premature aging in
patients with WS.

end excerpt

Further evidence that the Werner's syndrome gene codes for a DNA
helicase appears in the August 1, 1997 edition of Nucleic Acids
Research Online. Article title : "DNA helicase activity in Werner's
syndrome gene product synthesized in a baculovirus system" by Noriyuki
Suzuki, Akira Shimamoto, Osamu Imamura, Junro Kuromitsu, Saori Kitao,
Makoto Goto1 and Yasuhiro Furuichi

http://www.oup.co.uk/oup/smj/journals/ed/titles/nar/Volume_25/Issue_15/gka505_gml.abs.html

begin excerpt

The gene responsible for Werner's syndrome (WRN) contains a region
homologous to the Escherichia coli RecQ type DNA helicase and was
thought to code for a DNA helicase belonging to this helicase
family. However, no evidence has been shown before to substantiate
this prediction. Here, we show data that the product of the WRN gene
is indeed a DNA helicase.

end excerpt

Switching topics. The topic of telomeres comes up on this list
periodically. Telomeres and telomerase are relevant to cancer
research, aging research, and cloning. Science News, October 11, 1997,
reports (based on an article in Cell) that telomerase-deficient mice
have been created and six generations have been bred.
The results are controversial. See:

http://www.sciencenews.org/sn_arc97/10_11_97/fob1.htm

Gregory Sullivan