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Titolo:
Involvement of Schizosaccharomyces pombe Srs2 in cellular responses to DNAdamage
Autore:
Wang, SW; Goodwin, A; Hickson, ID; Norbury, CJ;
Indirizzi:
Univ Oxford, John Radcliffe Hosp,Weatherall Inst Mol Med, Imperial Canc Res Fund, Oncol Mol Lab, Oxford OX3 9DS, England Univ Oxford Oxford EnglandOX3 9DS ncol Mol Lab, Oxford OX3 9DS, England
Titolo Testata:
NUCLEIC ACIDS RESEARCH
fascicolo: 14, volume: 29, anno: 2001,
pagine: 2963 - 2972
SICI:
0305-1048(20010715)29:14<2963:IOSPSI>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
WERNERS-SYNDROME GENES; HUMAN RAD52 PROTEIN; SACCHAROMYCES-CEREVISIAE; BLOOMS-SYNDROME; HOMOLOGOUS RECOMBINATION; HELICASE; YEAST; REPLICATION; REPAIR; CHECKPOINT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Norbury, CJ Univ Oxford, John Radcliffe Hosp,Weatherall Inst Mol Med, Imperial Canc Res Fund, Oncol Mol Lab, Oxford OX3 9DS, England Univ Oxford Oxford England OX3 9DS , Oxford OX3 9DS, England
Citazione:
S.W. Wang et al., "Involvement of Schizosaccharomyces pombe Srs2 in cellular responses to DNAdamage", NUCL ACID R, 29(14), 2001, pp. 2963-2972

Abstract

In the budding yeast Saccharomyces cerevisiae the Srs2/RadH DNA helicase promotes survival after ultraviolet (UV) irradiation, and has been implicated in DNA repair, recombination and checkpoint signalling following DNA damage. A second helicase, Sgs1, is the S. cerevisiae homologue of the human BLM and WRN proteins, which are defective in cancer predisposition and/or premature ageing syndromes. Saccharomyces cerevisiae cells lacking both Srs2 and Sgs1 exhibit a severe growth defect. We have identified an Srs2 orthologue in the fission: yeast Schizosaccharomyces pombe, and have investigated its role in responses to UV irradiation and inhibition of DNA replication. Deletion of fission yeast srs2 caused spontaneous hyper-recombination and UVsensitivity, and simultaneous deletion of the SGS1 homologue rqh1 caused asevere growth defect reminiscent of that seen in the equivalent S. cerevisiae mutant. However, unlike in budding yeast, inactivation of the homologous recombination pathway did not suppress this growth defect. Indeed, the homologous recombination pathway was required for maintenance of normal fission yeast viability in the absence of Srs2, and loss of homologous recombination and loss of Srs2 contributed additively to UV sensitivity. We concludethat Srs2 plays related, but not identical, roles in the two yeast species.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 16:15:35