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Human RECQ5 helicase promotes repair of DNA double-strand breaks by synthesis-dependent strand annealing
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SYSNO ASEP 0436398 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název Human RECQ5 helicase promotes repair of DNA double-strand breaks by synthesis-dependent strand annealing Tvůrce(i) Paliwal, S. (CH)
Kanagaraj, R. (CH)
Sturzenegger, A. (CH)
Burdová, Kamila (UMG-J)
Janščák, Pavel (UMG-J) RIDZdroj.dok. Nucleic Acids Research. - : Oxford University Press - ISSN 0305-1048
Roč. 42, č. 4 (2014), s. 2380-2390Poč.str. 11 s. Jazyk dok. eng - angličtina Země vyd. GB - Velká Británie Klíč. slova Human RECQ5 helicase ; DNA double-strand breaks ; mitotic homologous recombination Vědní obor RIV EB - Genetika a molekulární biologie CEP GA204/09/0565 GA ČR - Grantová agentura ČR GAP305/10/0281 GA ČR - Grantová agentura ČR Institucionální podpora UMG-J - RVO:68378050 UT WOS 000332381000032 DOI 10.1093/nar/gkt1263 Anotace Most mitotic homologous recombination (HR) events proceed via a synthesis-dependent strand annealing mechanism to avoid crossing over, which may give rise to chromosomal rearrangements and loss of heterozygosity. The molecular mechanisms controlling HR sub-pathway choice are poorly understood. Here, we show that human RECQ5, a DNA helicase that can disrupt RAD51 nucleoprotein filaments, promotes formation of non-crossover products during DNA double-strand break-induced HR and counteracts the inhibitory effect of RAD51 on RAD52-mediated DNA annealing in vitro and in vivo. Moreover, we demonstrate that RECQ5 deficiency is associated with an increased occupancy of RAD51 at a double-strand break site, and it also causes an elevation of sister chromatid exchanges on inactivation of the Holliday junction dissolution pathway or on induction of a high load of DNA damage in the cell. Collectively, our findings suggest that RECQ5 acts during the post-synaptic phase of synthesis-dependent strand annealing to prevent formation of aberrant RAD51 filaments on the extended invading strand, thus limiting its channeling into potentially hazardous crossover pathway of HR. Pracoviště Ústav molekulární genetiky Kontakt Nikol Škňouřilová, nikol.sknourilova@img.cas.cz, Tel.: 241 063 217 Rok sběru 2015
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