Nature Genetics
25, 192 - 194 (2000)
doi:10.1038/76055
Homologous recombination is responsible for cell death in the absence
of the Sgs1 and Srs2 helicasesSerge Gangloff, Christine Soustelle
& Francis Fabre
CEA de Fontenay-aux-Roses, UMR 217 CNRS−CEA/DSV/DRR/LERA
, 92265 Fontenay-aux-Roses, France.
Correspondence should be addressed to Serge Gangloff Serge.Gangloff@cea.fr or or Francis Fabre Francis.Fabre@cea.frDNA helicases are involved in many aspects of DNA metabolism, including
transcription, replication, recombination and repair. In the yeast Saccharomyces
cerevisiae, the absence of the Sgs1 helicase results in genomic instability
and accelerated ageing1,
2,
3,
4. In human cells, mutations
in orthologues of SGS1 lead to Bloom (BS), Werner (WS) or Rothmund-Thomson
(RTS) syndromes, which are rare, autosomal recessive diseases characterized
by genetic instability associated with cancer predisposition5,
6,
7.
Although data concerning these human diseases are accumulating, there is still
no clear idea of the function of the proteins involved. Here we show that
sgs1 mutants are deficient in DNA repair and are defective for
induced recombination events that involve homologous chromosomes. The role
of homologous recombination is further evidenced in haploid cells in which
both Sgs1p and Srs2p are absent. Yeast SRS2 encodes another DNA helicase
involved in the maintenance of genome integrity8,
9,
10. Our
data suggest that some defects observed in BS, WS or RTS are the consequence
of unrestrained recombination.
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