MCM9 Is Required for Mammalian DNA Mismatch Repair
作者： Sabine Traver , Philippe Coulombe , Isabelle Peiffer , James R.A. Hutchins , Magali Kitzmann
DOI: 10.1016/J.MOLCEL.2015.07.010
关键词: DNA mismatch repair 、 DNA polymerase 、 Genetics 、 Homologous recombination 、 Biology 、 Chromatin 、 MSH2 、 Helicase 、 MSH3 、 Microsatellite instability
摘要: DNA mismatch repair (MMR) is an evolutionarily conserved process that corrects polymerase errors during replication to maintain genomic integrity. In E. coli, the helicase UvrD implicated in MMR, yet analogous activity has not been identified eukaryotes. Here, we show mammalian MCM9, a protein involved and homologous recombination, forms complex with MMR initiation proteins (MSH2, MSH3, MLH1, PMS1, clamp loader RFC) essential for MMR. Mcm9-/- cells display microsatellite instability deficiency. The MCM9 required efficient since wild-type but helicase-dead restores cells. Moreover, loading onto chromatin MSH2-dependent, turn stimulates recruitment of MLH1 chromatin. Our results reveal role its
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