RecA protein promotes the regression of stalled replication forks in vitro.
Replication forks are halted by many types of DNA damage. At the site of a leading-strand DNA lesion, forks may stall and leave the lesion in a single-strand gap. Fork regression is the first step in several proposed pathways that permit repair without generating a double-strand break. Using model DNA substrates designed to mimic one of the known structures of a fork stalled at a leading-strand lesion, we show here that RecA protein of Escherichia coli will promote a fork regression reaction in vitro. The regression process exhibits an absolute requirement for ATP hydrolysis and is enhanced when dATP replaces ATP. The reaction is not affected by the inclusion of the RecO and R proteins. We present this reaction as one of several potential RecA protein roles in the repair of stalled and/or collapsed replication forks in bacteria.
Robu
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ME
Department of Biochemistry, University of Wisconsin, Madison, WI 53706-1544, USA.
Inman
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RB
Cox
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D004261:DNA Replication; D004270:DNA, Circular / Q000096:biosynthesis; D004277:DNA, Single-Stranded / Q000096:biosynthesis; D004279:DNA, Viral / Q000096:biosynthesis*; D004926:Escherichia coli / Q000235:genetics; D011938:Rec A Recombinases / Q000378:metabolism*
D004270:DNA, Circular; D004277:DNA, Single-Stranded; D004279:DNA, Viral; D011938:Rec A Recombinases