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DNA helicase Srs2 disrupts the Rad51 presynaptic filament.
Krejci L, Van Komen S, Li Y, Villemain J, Reddy MS, Klein H, Ellenberger T, Sung P
Nature 2003 May 15 423(6937):305-9 [abstract on PubMed] [related articles] [order article]
Selected by | Antony Carr / Dale Ramsden
First evaluation 6 Jun 2003 | Latest evaluation 18 Jun 2003
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Antony Carr
University of Sussex, United Kingdom
CELL BIOLOGY

New Finding
This paper elucidates the role played by Srs2 helicase in negatively regulating recombination in yeast cells. In vitro, purified Srs2 helicase reverses the formation of Rad51 filaments. In addition, loss of Srs2 in yeast cells causes a hyper-recombination phenotype and under specific circumstances appears to prevent cells from completing repair. These data, together with those from Veaute et al. (Nature 2003, 423:309 [PMID: 12748645]), provide mechanistic insight into srs2 mutant phenotypes.

Evaluated 18 Jun 2003
Dale Ramsden
0, United States
STRUCTURAL BIOLOGY

Hypothesis
New Finding
Krejci et al (and a similar work by Veaute et al {1} published in the same issue) provide a satisfying mechanistic explanation for the "anti-recombination" activity of certain DNA helicases. They show that the yeast DNA helicase SRS2 disrupts protein-DNA filaments containing rad51 and ssDNA, a critical intermediate in recombination. {1} Veaute et al. Nature 2003, 423:309-12 [PMID:12748645].

Evaluated 6 Jun 2003
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