Malkova A, Signon L, Schaefer C B, Naylor M L, Theis J F, Newlon C S, Haber J E
Rosenstiel Center and Department of Biology, Brandeis University, Waltham, Massachusetts 02254-9110, USA.
Genes Dev. 2001 May 1;15(9):1055-60. doi: 10.1101/gad.875901.
Without the RAD51 strand exchange protein, Saccharomyces cerevisiae cannot repair a double-strand break (DSB) by gene conversion. However, cells can repair DSBs by recombination-dependent, break-induced replication (BIR). RAD51-independent BIR is initiated more than 13 kb from the DSB. Repair depends on a 200-bp sequence adjacent to ARS310, located approximately 34 kb centromere-proximal to the DSB, but does not depend on the origin activity of ARS310. We conclude that the ability of a recombination-induced replication fork to copy > 130 kb to the end of the chromosome depends on a special site that enhances assembly of a processive repair replication fork.
没有RAD51链交换蛋白,酿酒酵母就无法通过基因转换修复双链断裂(DSB)。然而,细胞可以通过依赖重组的断裂诱导复制(BIR)来修复DSB。不依赖RAD51的BIR在距离DSB超过13 kb处启动。修复依赖于与ARS310相邻的200 bp序列,该序列位于距离DSB着丝粒近端约34 kb处,但不依赖于ARS310的起始活性。我们得出结论,重组诱导的复制叉将> 130 kb复制到染色体末端的能力取决于一个特殊位点,该位点可增强持续性修复复制叉的组装。