作者: Chun-Chin Chen , Elena Avdievich , Yongwei Zhang , Yu Zhang , Kaichun Wei
DOI: 10.1016/J.DNAREP.2017.07.003
关键词:
摘要: Abstract DNA double-strand breaks (DSBs) can be repaired through several mechanisms, including homologous recombination (HR). While HR between identical sequences is robust in mammalian cells, diverged suppressed by mismatch-repair (MMR) components such as MSH2. Exonuclease I (EXO1) interacts with the MMR machinery and has been proposed to act downstream of mismatch recognition proteins correction. EXO1 also shown participate extensive DSB end resection, an initial step pathway. To assess contribution DSB-inducible reporters were introduced into Exo1−/− mouse embryonic stem a novel GFP reporter containing silent polymorphisms monitor sequences. Compared which was not clearly affected, substantially increased cells although lesser extent than seen Msh2−/− cells. Thus, like canonical proteins, restrain aberrant events sequence elements genome.