DNA repair: Rad52 – the means to an end
نویسنده
چکیده
In eukaryotic organisms, double-strand breaks in chromosomal DNA are repaired either by non-homologous end-joining, or by homologous recombination. How do cells choose which pathway to use?
منابع مشابه
Rad52 promotes second-end DNA capture in double-stranded break repair to form complement-stabilized joint molecules.
Saccharomyces cerevisiae Rad52 performs multiple functions during the recombinational repair of double-stranded DNA (dsDNA) breaks (DSBs). It mediates assembly of Rad51 onto single-stranded DNA (ssDNA) that is complexed with replication protein A (RPA); the resulting nucleoprotein filament pairs with homologous dsDNA to form joint molecules. Rad52 also catalyzes the annealing of complementary s...
متن کاملRad51 protein controls Rad52-mediated DNA annealing.
In Saccharomyces cerevisiae, Rad52 protein plays an essential role in the repair of DNA double-stranded breaks (DSBs). Rad52 and its orthologs possess the unique capacity to anneal single-stranded DNA (ssDNA) complexed with its cognate ssDNA-binding protein, RPA. This annealing activity is used in multiple mechanisms of DSB repair: single-stranded annealing, synthesis-dependent strand annealing...
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Reverse transcription of retroviral RNA into linear double-stranded DNA and its integration into the host cell genome are essential steps in the retroviral life cycle. The nonhomologous end-joining (NHEJ) DNA repair pathway has been implicated in protecting cells from retrovirus-induced apoptosis caused by strand breaks in host cell DNA or unintegrated linear viral DNA. In eukaryotes, both the ...
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Human RAD52 promotes annealing of complementary single-stranded DNA (ssDNA). In-depth knowledge of RAD52-DNA interaction is required to understand how its activity is integrated in DNA repair processes. Here, we visualize individual fluorescent RAD52 complexes interacting with single DNA molecules. The interaction with ssDNA is rapid, static, and tight, where ssDNA appears to wrap around RAD52 ...
متن کاملDNA damage-inducible and RAD52-independent repair of DNA double-strand breaks in Saccharomyces cerevisiae.
Chromosomal repair was studied in stationary-phase Saccharomyces cerevisiae, including rad52/rad52 mutant strains deficient in repairing double-strand breaks (DSBs) by homologous recombination. Mutant strains suffered more chromosomal fragmentation than RAD52/RAD52 strains after treatments with cobalt-60 gamma irradiation or radiomimetic bleomycin, except after high bleomycin doses when chromos...
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ورودعنوان ژورنال:
- Current Biology
دوره 9 شماره
صفحات -
تاریخ انتشار 1999