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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]
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Selected by
| Antony Carr / Dale Ramsden
First evaluation 6 Jun 2003 |
Latest evaluation 18 Jun 2003
 Relevant Sections
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| Faculty Comments |
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| Faculty
Member |
Comments |
Antony Carr
University of
Sussex, United Kingdom
CELL BIOLOGY
 New
Finding
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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.
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Evaluated
18 Jun 2003 |
Dale Ramsden
0, United
States
STRUCTURAL BIOLOGY
 Hypothesis
New Finding
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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 | | |
| Faculty Comments |
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