Homologous recombination is responsible for cell death in the absence of the Sgs1 and Srs2 helicases

Citation
S. Gangloff et al., Homologous recombination is responsible for cell death in the absence of the Sgs1 and Srs2 helicases, NAT GENET, 25(2), 2000, pp. 192-194
Citations number
26
Categorie Soggetti
Molecular Biology & Genetics
Journal title
NATURE GENETICS
ISSN journal
10614036 → ACNP
Volume
25
Issue
2
Year of publication
2000
Pages
192 - 194
Database
ISI
SICI code
1061-4036(200006)25:2<192:HRIRFC>2.0.ZU;2-D
Abstract
DNA helicases are involved in many aspects of DNA metabolism, including tra nscription, replication, recombination and repair. In the yeast Saccharomyc es cerevisiae, the absence of the Sgs1 helicase results in genomic instabil ity and accelerated ageing(1-4). In human cells, mutations in orthologues o f SGS1 lead to Bloom (BS). Werner (WS) or Rothmund-Thomson (RTS) syndromes, which are rare, autosomal recessive diseases characterized by genetic inst ability associated with cancer predisposition(5-7). Although data concernin g these human diseases are accumulating, there is still no clear idea of th e function of the proteins involved. Here we show that sgs1 Delta mutants a re deficient in DNA repair and are defective for induced recombination even ts that involve homologous chromosomes. The role of homologous recombinatio n is further evidenced in haploid cells in which both Sgs1p and Srs2p are a bsent. Yeast SRS2 encodes another DNA helicase involved in the maintenance of genome integrity(8-10). Our data suggest that some defects observed in B S. WS or RTS are the consequence of unrestrained recombination.