Role of Saw1 in Rad1/Rad10 complex assembly at recombination intermediates in budding yeast

Li, Fuyang; Dong, Junachao; Eichmiller, Robin; Holland, Cory; Minca, Eugen C.; Prakash, Rohit; Sung, Patrick; Shim, Eun Yong; Surtees, Jennifer A.; Lee, Sang Eun

doi:10.1038/emboj.2012.345

Cited by 36 publications

(111 citation statements)

References 47 publications

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“…We examined whether SSA and BIR could contribute to the Rad52-dependent suppression of dna2-K1080E and found that the deletion of Rad10, Saw1, and Tid1, important factors for SSA or BIR (76,98,99), did not affect the suppression (data not shown). It has also been shown that a subset of SCR events, which is facilitated by the RSC complex, could occur independently of Rad51 (78,79).…”

Section: Discussionmentioning

confidence: 99%

Rad52/Rad59-dependent Recombination as a Means to Rectify Faulty Okazaki Fragment Processing

Lee

Demin

et al. 2014

Journal of Biological Chemistry

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Background: How faulty Okazaki fragments are repaired remains unclear. Results: The DNA annealing activity of Rad52 and sister chromatid cohesion are important in the repair of faulty Okazaki fragments. Conclusion: Rad52/Rad59-mediated sister chromatid recombination is a major means of repairing faulty Okazaki fragments. Significance: The faithful repair of faulty Okazaki fragments is critical for genome stability.

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Section: Discussionmentioning

confidence: 99%

Rad52/Rad59-dependent Recombination as a Means to Rectify Faulty Okazaki Fragment Processing

Lee

Demin

et al. 2014

Journal of Biological Chemistry

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“…Therefore the 3′ NHTs must be removed to allow synthesis and subsequent ligation. Rad1-Rad10 is responsible for cleaving the tails, but requires partner proteins Msh2-Msh3 and Saw1 to be recruited to the 3′ NHTs [17, 19, 20]. Msh2-Msh3 has been proposed to stabilize the recombination intermediate to promote cleavage by Rad1-Rad10 [17, 20].…”

Section: Introductionmentioning

confidence: 99%

ATP binding and hydrolysis by Saccharomyces cerevisiae Msh2–Msh3 are differentially modulated by mismatch and double-strand break repair DNA substrates

et al. 2014

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In Saccharomyces cerevisiae, Msh2-Msh3-mediated mismatch repair (MMR) recognizes and targets insertion/deletion loops for repair. Msh2-Msh3 is also required for 3′ non-homologous tail removal (3′NHTR) in double-strand break repair. In both pathways, Msh2-Msh3 binds double-strand/single-strand junctions and initiates repair in an ATP-dependent manner. However, we recently demonstrated that the two pathways have distinct requirements with respect to Msh2-Msh3 activities. We identified a set of aromatic residues in the nucleotide binding pocket (FLY motif) of Msh3 that, when mutated, disrupted MMR, but left 3′ NHTR largely intact. One of these mutations, msh3Y942A, was predicted to disrupt the nucleotide sandwich and allow altered positioning of ATP within the pocket. To develop a mechanistic understanding of the differential requirements for ATP binding and/or hydrolysis in the two pathways, we characterized Msh2-Msh3 and Msh2-msh3Y942A ATP binding and hydrolysis activities in the presence of MMR and 3′ NHTR DNA substrates. We observed distinct, substrate-dependent ATP hydrolysis and nucleotide turnover by Msh2-Msh3, indicating that the MMR and 3′ NHTR DNA substrates differentially modify the ATP binding/hydrolysis activities of Msh2-Msh3. Msh2-msh3Y942A retained the ability to bind DNA and ATP but exhibited altered ATP hydrolysis and nucleotide turnover. We propose that both ATP and structure-specific repair substrates cooperate to direct Msh2-Msh3-mediated repair and suggest an explanation for the msh3Y942A separation-of-function phenotype.

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“…ChIP analysis revealed that SAW1 is required to recruit Rad1 to sites of SSA repair, indicating SAW1 function precedes flap trimming by the Rad1-Rad10 endonuclease in SSA [11]. A recent report showed that Saw1 has intrinsic affinity for flap and splayed arm DNAs and that binding of Saw1 to Rad1-Rad10 increases the affinity of Rad1-Rad10 binding to flap DNAs, especially those containing longer 3′ flaps [12]. A purified complex containing Saw1, Rad1 and Rad10 cleaves specific flap DNA structures in vitro [12].…”

Section: Introductionmentioning

confidence: 99%

SAW1 is required for SDSA double-strand break repair in S. cerevisiae

Diamante

Phan

Celis

et al. 2014

Biochemical and Biophysical Research Communications

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SAW1 , coding for Saw1, is required for single-strand annealing (SSA) DNA Double-strand Break (DSB) Repair in S. cerevisiae. Saw1 physically associates with Rad1 and Rad52 and recruits the Rad1-Rad10 endonuclease. Herein we show by fluorescence microscopy that SAW1 is similarly required for recruitment of Rad10 to sites of Synthesis-Dependent Strand Annealing (SDSA) and associates with sites of SDSA repair in a manner temporally overlapped with Rad10. The magnitude of induction of colocalized Saw1-CFP/Rad10-YFP/DSB-RFP foci in SDSA is more dramatic in S and G2 phase cells than in M phase, consistent with the known mechanism of SDSA. We observed a substantial fraction of foci in which Rad10 was localized to the repair site without Saw1, but few DSB sites that contained Saw1 without Rad10. Together these data are consistent with a model in which Saw1 recruits Rad1-Rad10 to SDSA sites, possibly even binding as a protein-protein complex, but departs the repair site in advance of Rad1-Rad10.

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Role of Saw1 in Rad1/Rad10 complex assembly at recombination intermediates in budding yeast

Cited by 36 publications

References 47 publications

Rad52/Rad59-dependent Recombination as a Means to Rectify Faulty Okazaki Fragment Processing

Rad52/Rad59-dependent Recombination as a Means to Rectify Faulty Okazaki Fragment Processing

ATP binding and hydrolysis by Saccharomyces cerevisiae Msh2–Msh3 are differentially modulated by mismatch and double-strand break repair DNA substrates

SAW1 is required for SDSA double-strand break repair in S. cerevisiae

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