Recovery from checkpoint-mediated arrest after repair of a double-strand break requires Srs2 helicase

Moreshwar B. Vaze; Achille Pellicioli; Sang Eun Lee; Grzegorz Ira; Giordano Liberi; Ayelet Arbel-Eden; Marco Foiani; James E. Haber

doi:10.1016/S1097-2765(02)00593-2

Recovery from checkpoint-mediated arrest after repair of a double-strand break requires Srs2 helicase

Moreshwar B. Vaze, Achille Pellicioli, Sang Eun Lee, Grzegorz Ira, Giordano Liberi, Ayelet Arbel-Eden, Marco Foiani, James E. Haber

Research output: Contribution to journal › Article › peer-review

278 Scopus citations

Abstract

In Saccharomyces strains in which homologous recombination is delayed sufficiently to activate the DNA damage checkpoint, Rad53p checkpoint kinase activity appears 1 hr after DSB induction and disappears soon after completion of repair. Cells lacking Srs2p helicase fail to recover even though they apparently complete DNA repair; Rad53p kinase remains activated. srs2Δ cells also fail to adapt when DSB repair is prevented. The recovery defect of srs2Δ is suppressed in mec1Δ strains lacking the checkpoint or when DSB repair occurs before checkpoint activation. Permanent preanaphase arrest of srs2Δ cells is reversed by the addition of caffeine after cells have arrested. Thus, in addition to its roles in recombination, Srs2p appears to be needed to turn off the DNA damage checkpoint.

Original language	English (US)
Pages (from-to)	373-385
Number of pages	13
Journal	Molecular Cell
Volume	10
Issue number	2
DOIs	https://doi.org/10.1016/S1097-2765(02)00593-2
State	Published - Aug 2002
Externally published	Yes

ASJC Scopus subject areas

Molecular Biology
Cell Biology

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title = "Recovery from checkpoint-mediated arrest after repair of a double-strand break requires Srs2 helicase",

abstract = "In Saccharomyces strains in which homologous recombination is delayed sufficiently to activate the DNA damage checkpoint, Rad53p checkpoint kinase activity appears 1 hr after DSB induction and disappears soon after completion of repair. Cells lacking Srs2p helicase fail to recover even though they apparently complete DNA repair; Rad53p kinase remains activated. srs2Δ cells also fail to adapt when DSB repair is prevented. The recovery defect of srs2Δ is suppressed in mec1Δ strains lacking the checkpoint or when DSB repair occurs before checkpoint activation. Permanent preanaphase arrest of srs2Δ cells is reversed by the addition of caffeine after cells have arrested. Thus, in addition to its roles in recombination, Srs2p appears to be needed to turn off the DNA damage checkpoint.",

author = "Vaze, {Moreshwar B.} and Achille Pellicioli and Lee, {Sang Eun} and Grzegorz Ira and Giordano Liberi and Ayelet Arbel-Eden and Marco Foiani and Haber, {James E.}",

note = "Funding Information: We are grateful to members of the Haber and Foiani labs for vigorous and helpful suggestions. We thank John McCusker and Ted Weinert for the gift of plasmids. We thank Eric Coic for the plasmid pEC1. Research was supported by grants from the Associazione Italiana per la Ricerca sul Cancro and from Telethon-Italy (Grant No. E.1108) to M.F. and NIH grants GM20056 and GM61766 and DOE grant 99ER62729 to J.E.H. S.E.L. is a recipient of a Hildegarde A. Becher Foundation senior fellowship of the Leukemia and Lymphoma Society.",

year = "2002",

month = aug,

doi = "10.1016/S1097-2765(02)00593-2",

language = "English (US)",

volume = "10",

pages = "373--385",

journal = "Molecular Cell",

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T1 - Recovery from checkpoint-mediated arrest after repair of a double-strand break requires Srs2 helicase

AU - Vaze, Moreshwar B.

AU - Pellicioli, Achille

AU - Lee, Sang Eun

AU - Ira, Grzegorz

AU - Liberi, Giordano

AU - Arbel-Eden, Ayelet

AU - Foiani, Marco

AU - Haber, James E.

N1 - Funding Information: We are grateful to members of the Haber and Foiani labs for vigorous and helpful suggestions. We thank John McCusker and Ted Weinert for the gift of plasmids. We thank Eric Coic for the plasmid pEC1. Research was supported by grants from the Associazione Italiana per la Ricerca sul Cancro and from Telethon-Italy (Grant No. E.1108) to M.F. and NIH grants GM20056 and GM61766 and DOE grant 99ER62729 to J.E.H. S.E.L. is a recipient of a Hildegarde A. Becher Foundation senior fellowship of the Leukemia and Lymphoma Society.

PY - 2002/8

Y1 - 2002/8

N2 - In Saccharomyces strains in which homologous recombination is delayed sufficiently to activate the DNA damage checkpoint, Rad53p checkpoint kinase activity appears 1 hr after DSB induction and disappears soon after completion of repair. Cells lacking Srs2p helicase fail to recover even though they apparently complete DNA repair; Rad53p kinase remains activated. srs2Δ cells also fail to adapt when DSB repair is prevented. The recovery defect of srs2Δ is suppressed in mec1Δ strains lacking the checkpoint or when DSB repair occurs before checkpoint activation. Permanent preanaphase arrest of srs2Δ cells is reversed by the addition of caffeine after cells have arrested. Thus, in addition to its roles in recombination, Srs2p appears to be needed to turn off the DNA damage checkpoint.

AB - In Saccharomyces strains in which homologous recombination is delayed sufficiently to activate the DNA damage checkpoint, Rad53p checkpoint kinase activity appears 1 hr after DSB induction and disappears soon after completion of repair. Cells lacking Srs2p helicase fail to recover even though they apparently complete DNA repair; Rad53p kinase remains activated. srs2Δ cells also fail to adapt when DSB repair is prevented. The recovery defect of srs2Δ is suppressed in mec1Δ strains lacking the checkpoint or when DSB repair occurs before checkpoint activation. Permanent preanaphase arrest of srs2Δ cells is reversed by the addition of caffeine after cells have arrested. Thus, in addition to its roles in recombination, Srs2p appears to be needed to turn off the DNA damage checkpoint.

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Recovery from checkpoint-mediated arrest after repair of a double-strand break requires Srs2 helicase

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