Werner's syndrome, Open for study

Jim Cummins cummins at possum.murdoch.edu.au
Tue Dec 28 20:11:17 EST 1993


Check out Thweatt R, Goldstein S (1993): Werner syndrome and biological
aging - a molecular genetic hypothesis. Bioessays 15:421-42

"Cultured fibroblasts derived from subjects with WS are found to
undergo premature replicative senescence and thus provide a cellular
model system to study the disorder. Recently, several overexpressed
gene sequences isolated from a WS fibroblast cDNA library have been
shown to possess the capacity to inhibit DNA synthesis and disrupt many
normal biochemical processes. Because a similar constellation of genes
is overexpressed in WS and senescent normal fibroblasts, these data
suggest the existence of a common molecular genetic pathway for
replicative senescence in both types of cell. We propose that the
primary defect in WS is a mutation in a gene for a trans-acting
repressor protein that reduces its binding affinity for shared
regulatory regions of several genes, including those that encode
inhibitors of DNA synthesis (IDS). The mutant WS repressor triggers a
sequence of premature expression of IDS and other genes, with resulting
inhibition of DNA synthesis and early cellular senescence, events which
occur much later in normal cells."

(from Medline)

Jim Cummins                   
School of Veterinary Studies
Murdoch University
Western Australia 6150  Tel +61-9-360 2668 Fax +61-9-310 4144
For every complex problem there's a simple solution.  And it's wrong!




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