X-Message-Number: 24220
Date: Wed, 9 Jun 2004 20:00:47 -0700 (PDT)
From: Doug Skrecky <>
Subject: no support for a telomere-independent mechanism of replicative aging.

Genes Dev. 2001 Feb 15;15(4):398-403
Putative telomere-independent mechanisms of replicative aging reflect
inadequate growth conditions.
  Telomere shortening is the mechanism underlying replicative aging in
fibroblasts. A variety of reports now claim that inactivation of the
p16(INK4a)/pRB pathway is required in addition to telomere maintenance
for the immortalization of cells such as skin keratinocytes and breast
epithelial cells. We here show that the premature growth arrest of these
cell types can be explained by an inadequate culture environment.
Providing mesenchymal/epithelial interactions by cultivating the
telomerase-expressing cells on feeder layers avoids the growth arrest
associated with increased p16(INK4a). These results do not support a
telomere-independent mechanism of replicative aging.

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