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Vol. 9, Issue 3, 611-621, March 1998
Department of Molecular Biology, Lundberg Laboratory,
Göteborg University, S-405 30 Göteborg, Sweden
We have studied telomere length in Schizosaccharomyces
pombe strains carrying mutations affecting cell cycle
checkpoints, DNA repair, and regulation of the Cdc2 protein kinase.
Telomere shortening was found in rad1,
rad3, rad17, and rad26
mutants. Telomere lengths in previously characterized
rad1 mutants paralleled the replication checkpoint
proficiency of those mutants. In contrast, rad9,
chk1, hus1, and cds1
mutants had intact telomeres. No difference in telomere length was seen
in mutants affected in the regulation of Cdc2, whereas some of the DNA
repair mutants examined had slightly longer telomeres than did the wild
type. Overexpression of the rad1+ gene
caused telomeres to elongate slightly. The kinetics of telomere shortening was monitored by following telomere length after disruption of the rad1+ gene; the rate was ~1
nucleotide per generation. Wild-type telomere length could be restored
by reintroduction of the wild-type rad1+
gene. Expression of the Saccharomyces cerevisiae RCK1
protein kinase gene, which suppresses the radiation and hydroxyurea
sensitivity of Sz. pombe checkpoint mutants, was able to
attenuate telomere shortening in rad1 mutant cells and
to increase telomere length in a wild-type background. The functional
effects of telomere shortening in rad1 mutants were
assayed by measuring loss of a linear and a circular minichromosome. A
minor increase in loss rate was seen with the linear minichromosome,
and an even smaller difference compared with wild-type was detected
with the circular plasmid.
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