In the budding yeast Saccharomyces cerevisiae the Srs2/RadH DNA helicase pr
omotes survival after ultraviolet (UV) irradiation, and has been implicated
in DNA repair, recombination and checkpoint signalling following DNA damag
e. A second helicase, Sgs1, is the S. cerevisiae homologue of the human BLM
and WRN proteins, which are defective in cancer predisposition and/or prem
ature ageing syndromes. Saccharomyces cerevisiae cells lacking both Srs2 an
d Sgs1 exhibit a severe growth defect. We have identified an Srs2 orthologu
e in the fission: yeast Schizosaccharomyces pombe, and have investigated it
s role in responses to UV irradiation and inhibition of DNA replication. De
letion of fission yeast srs2 caused spontaneous hyper-recombination and UV
sensitivity, and simultaneous deletion of the SGS1 homologue rqh1 caused a
severe growth defect reminiscent of that seen in the equivalent S. cerevisi
ae mutant. However, unlike in budding yeast, inactivation of the homologous
recombination pathway did not suppress this growth defect. Indeed, the hom
ologous recombination pathway was required for maintenance of normal fissio
n yeast viability in the absence of Srs2, and loss of homologous recombinat
ion and loss of Srs2 contributed additively to UV sensitivity. We conclude
that Srs2 plays related, but not identical, roles in the two yeast species.