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Vol. 13, Issue 8, 2626-2638, August 2002
Department of Genetics, Cell Biology and Development, University of
Minnesota, St. Paul, Minnesota 55108
When telomerase is absent and/or telomeres become critically short,
cells undergo a progressive decline in viability termed senescence. The
telomere checkpoint model predicts that cells will respond to a damaged
or critically short telomere by transiently arresting and activating
repair of the telomere. We examined the senescence of
telomerase-deficient Saccharomyces cerevisiae at the
cellular level to ask if the loss of telomerase activity triggers a
checkpoint response. As telomerase-deficient mutants were serially subcultured, cells exhibited a progressive decline in average growth
rate and an increase in the number of cells delayed in the G2/M stage
of the cell cycle. MEC3, MEC1, and
DDC2, genes important for the DNA damage checkpoint
response, were required for the cell cycle delay in
telomerase-deficient cells. In contrast, TEL1,
RAD9, and RAD53, genes also required for
the DNA damage checkpoint response, were not required for the G2/M
delay in telomerase-deficient cells. We propose that the telomere
checkpoint is distinct from the DNA damage checkpoint and requires a
specific set of gene products to delay the cell cycle and presumably to
activate telomerase and/or other telomere repair activities.
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