Budding yeast Mms22 and Mms1 regulate homologous recombination induced by replisome blockage

Eris Duro, Jessica A. Vaisica, Grant W. Brown, John Rouse

    Research output: Contribution to journalArticle

    46 Citations (Scopus)

    Abstract

    Yeast cells lacking MMS22 or MMS1 are hypersensitive to agents that perturb replisome progression but the cellular functions of these genes are unknown. In this study we investigate the involvement of budding yeast MMS22 and MMS1 in homologous recombination (HR). Recombination between sister chromatids or between homologous chromosomes induced by agents that block replisomes was severely defective in cells lacking MMS22 or MMS1. In contrast, HR induced by double-strand breaks was not affected by the absence of these genes. Major defects in MMS-induced HR were also observed in cells lacking the cullin RTT101, the histone acetyltransferase RTT109 and in cells lacking the histone chaperone ASF1, all of which interact genetically with MMS22 and MMS1. Finally, we show that cells lacking either MMS22 or MMS1 are defective in recovery from MMS-induced replisome stalling. These results identify Mms22 and Mms1 as S-phase specific recombination-promoting factors. (c) 2008 Elsevier B.V. All rights reserved.

    Original languageEnglish
    Pages (from-to)811-818
    Number of pages8
    JournalDNA Repair
    Volume7
    Issue number5
    DOIs
    Publication statusPublished - 3 May 2008

    Cite this

    Duro, Eris ; Vaisica, Jessica A. ; Brown, Grant W. ; Rouse, John. / Budding yeast Mms22 and Mms1 regulate homologous recombination induced by replisome blockage. In: DNA Repair. 2008 ; Vol. 7, No. 5. pp. 811-818.
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    abstract = "Yeast cells lacking MMS22 or MMS1 are hypersensitive to agents that perturb replisome progression but the cellular functions of these genes are unknown. In this study we investigate the involvement of budding yeast MMS22 and MMS1 in homologous recombination (HR). Recombination between sister chromatids or between homologous chromosomes induced by agents that block replisomes was severely defective in cells lacking MMS22 or MMS1. In contrast, HR induced by double-strand breaks was not affected by the absence of these genes. Major defects in MMS-induced HR were also observed in cells lacking the cullin RTT101, the histone acetyltransferase RTT109 and in cells lacking the histone chaperone ASF1, all of which interact genetically with MMS22 and MMS1. Finally, we show that cells lacking either MMS22 or MMS1 are defective in recovery from MMS-induced replisome stalling. These results identify Mms22 and Mms1 as S-phase specific recombination-promoting factors. (c) 2008 Elsevier B.V. All rights reserved.",
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    Budding yeast Mms22 and Mms1 regulate homologous recombination induced by replisome blockage. / Duro, Eris; Vaisica, Jessica A.; Brown, Grant W.; Rouse, John.

    In: DNA Repair, Vol. 7, No. 5, 03.05.2008, p. 811-818.

    Research output: Contribution to journalArticle

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    AU - Vaisica, Jessica A.

    AU - Brown, Grant W.

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    AB - Yeast cells lacking MMS22 or MMS1 are hypersensitive to agents that perturb replisome progression but the cellular functions of these genes are unknown. In this study we investigate the involvement of budding yeast MMS22 and MMS1 in homologous recombination (HR). Recombination between sister chromatids or between homologous chromosomes induced by agents that block replisomes was severely defective in cells lacking MMS22 or MMS1. In contrast, HR induced by double-strand breaks was not affected by the absence of these genes. Major defects in MMS-induced HR were also observed in cells lacking the cullin RTT101, the histone acetyltransferase RTT109 and in cells lacking the histone chaperone ASF1, all of which interact genetically with MMS22 and MMS1. Finally, we show that cells lacking either MMS22 or MMS1 are defective in recovery from MMS-induced replisome stalling. These results identify Mms22 and Mms1 as S-phase specific recombination-promoting factors. (c) 2008 Elsevier B.V. All rights reserved.

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