DNA helicase Srs2 disrupts the Rad51 presynaptic filament.

J 2003

DNA helicase Srs2 disrupts the Rad51 presynaptic filament.

KREJČÍ, Lumír, Stephen VAN KOMEN, Ying LI, Jane VILLEMAIN, Sredhar REDDY et. al.

Základní údaje

Originální název

DNA helicase Srs2 disrupts the Rad51 presynaptic filament.

Název česky

DNA helicase Srs2 disrupts the Rad51 presynaptic filament.

Autoři

KREJČÍ, Lumír (203 Česká republika, garant), Stephen VAN KOMEN (840 Spojené státy), Ying LI (840 Spojené státy), Jane VILLEMAIN (840 Spojené státy), Sredhar REDDY (356 Indie), Hannah KLEIN (840 Spojené státy), Tom ELLENBERGER (840 Spojené státy) a Patrick SUNG (840 Spojené státy)

Vydání

Nature, Lodon, UK, Nature Publishing Group, 2003, 0028-0836

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

10600 1.6 Biological sciences

Stát vydavatele

Spojené státy

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 30.979

Organizační jednotka

Přírodovědecká fakulta

Klíčová slova anglicky

recombination; repair; Srs2;Rad51

Štítky

Rad51, recombination, repair, Srs2

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 15. 5. 2009 22:59, doc. Mgr. Lumír Krejčí, Ph.D.

Anotace

ORIG CZ

V originále

Mutations in the Saccharomyces cerevisiae gene SRS2 result in the yeast's sensitivity to genotoxic agents, failure to recover or adapt from DNA damage checkpoint-mediated cell cycle arrest, slow growth, chromosome loss, and hyper-recombination. Furthermore, double mutant strains, with mutations in DNA helicase genes SRS2 and SGS1, show low viability that can be overcome by inactivating recombination, implying that untimely recombination is the cause of growth impairment. Here we clarify the role of SRS2 in recombination modulation by purifying its encoded product and examining its interactions with the Rad51 recombinase. Srs2 has a robust ATPase activity that is dependent on single-stranded DNA (ssDNA) and binds Rad51, but the addition of a catalytic quantity of Srs2 to Rad51-mediated recombination reactions causes severe inhibition of these reactions. We show that Srs2 acts by dislodging Rad51 from ssDNA. Thus, the attenuation of recombination efficiency by Srs2 stems primarily from its ability to dismantle the Rad51 presynaptic filament efficiently. Our findings have implications for the basis of Bloom's and Werner's syndromes, which are caused by mutations in DNA helicases and are characterized by increased frequencies of recombination and a predisposition to cancers and accelerated ageing.

Česky

Srs2 a jeho anti-rekombinační aktivita

Citovat

KREJČÍ, Lumír, Stephen VAN KOMEN, Ying LI, Jane VILLEMAIN, Sredhar REDDY, Hannah KLEIN, Tom ELLENBERGER a Patrick SUNG. DNA helicase Srs2 disrupts the Rad51 presynaptic filament. Nature. Lodon, UK: Nature Publishing Group, 2003, roč. 423, č. 6937, s. 305-9, 4 s. ISSN 0028-0836.

@article{708586,
   author = {Krejčí, Lumír and Van Komen, Stephen and Li, Ying and Villemain, Jane and Reddy, Sredhar and Klein, Hannah and Ellenberger, Tom and Sung, Patrick},
   article_location = {Lodon, UK},
   article_number = {6937},
   keywords = {recombination; repair; Srs2;Rad51},
   language = {eng},
   issn = {0028-0836},
   journal = {Nature},
   title = {DNA helicase Srs2 disrupts the Rad51 presynaptic filament.},
   volume = {423},
   year = {2003}
}

TY  - JOUR
ID  - 708586
AU  - Krejčí, Lumír - Van Komen, Stephen - Li, Ying - Villemain, Jane - Reddy, Sredhar - Klein, Hannah - Ellenberger, Tom - Sung, Patrick
PY  - 2003
TI  - DNA helicase Srs2 disrupts the Rad51 presynaptic filament.
JF  - Nature
VL  - 423
IS  - 6937
SP  - 305-9
EP  - 305-9
PB  - Nature Publishing Group
SN  - 00280836
KW  - recombination
KW  - repair
KW  - Srs2;Rad51
N2  - Mutations in the Saccharomyces cerevisiae gene SRS2 result in the yeast's sensitivity to genotoxic agents, failure to recover or adapt from DNA damage checkpoint-mediated cell cycle arrest, slow growth, chromosome loss, and hyper-recombination. Furthermore, double mutant strains, with mutations in DNA helicase genes SRS2 and SGS1, show low viability that can be overcome by inactivating recombination, implying that untimely recombination is the cause of growth impairment. Here we clarify the role of SRS2 in recombination modulation by purifying its encoded product and examining its interactions with the Rad51 recombinase. Srs2 has a robust ATPase activity that is dependent on single-stranded DNA (ssDNA) and binds Rad51, but the addition of a catalytic quantity of Srs2 to Rad51-mediated recombination reactions causes severe inhibition of these reactions. We show that Srs2 acts by dislodging Rad51 from ssDNA. Thus, the attenuation of recombination efficiency by Srs2 stems primarily from its ability to dismantle the Rad51 presynaptic filament efficiently. Our findings have implications for the basis of Bloom's and Werner's syndromes, which are caused by mutations in DNA helicases and are characterized by increased frequencies of recombination and a predisposition to cancers and accelerated ageing.
ER  -

KREJČÍ, Lumír, Stephen VAN KOMEN, Ying LI, Jane VILLEMAIN, Sredhar REDDY, Hannah KLEIN, Tom ELLENBERGER a Patrick SUNG. DNA helicase Srs2 disrupts the Rad51 presynaptic filament. \textit{Nature}. Lodon, UK: Nature Publishing Group, 2003, roč.~423, č.~6937, s.~305-9, 4 s. ISSN~0028-0836.

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