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Putnam CD, et al.  (2010) Post-replication repair suppresses duplication-mediated genome instability. PLoS Genet 6():e1000933

Abstract: RAD6 is known to suppress duplication-mediated gross chromosomal rearrangements (GCRs) but not single-copy sequence mediated GCRs. Here, we found that the RAD6- and RAD18-dependent post-replication repair (PRR) and the RAD5-, MMS2-, UBC13-dependent error-free PRR branch acted in concert with the replication stress checkpoint to suppress duplication-mediated GCRs formed by homologous recombination (HR). The Rad5 helicase activity, but not its RING finger, was required to prevent duplication-mediated GCRs, although the function of Rad5 remained dependent upon modification of PCNA at Lys164. The SRS2, SGS1, and HCS1 encoded helicases appeared to interact with Rad5, and epistasis analysis suggested that Srs2 and Hcs1 act upstream of Rad5. In contrast, Sgs1 likely functions downstream of Rad5, potentially by resolving DNA structures formed by Rad5. Our analysis is consistent with models in which PRR prevents replication damage from becoming double strand breaks (DSBs) and/or regulates the activity of HR on DSBs.

Status: Published Type: Journal Article | Research Support, N.I.H., Extramural PubMed ID: 20463880

Topics addressed in this paper

Number of different genes curated to this paper: 30

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Topics Genes linked to topics (#1 - 10 )
BRE1 HCS1 HRQ1 IRC20 LGE1 MEC1 MGS1 MMS2 MPH1 MRC1
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Topics Genes linked to topics (#11 - 20 )
PIF1 POL30 RAD18 RAD30 RAD5 RAD52 RAD53 RAD6 RAD9 REV3
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Topics Genes linked to topics (#21 - 30 )
RRM3 SGS1 SIZ1 SML1 SRS2 TAF14 TOF1 TSA1 UBC13 UBR1
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