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Roles for mismatch repair family proteins in promoting meiotic crossing over
Institution:1. Institute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Université Paris-Sud, Université Paris-Saclay, 91198, Gif-sur-Yvette cedex, France;2. Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA;1. Department of Medical Genetics, School of Basic Medical Sciences, Wuhan University, Wuhan 430071, China;2. Department of Biochemistry and Molecular Biology, Norris Comprehensive Cancer Center, University of Southern CA Keck School of Medicine, Los Angeles, CA 90033, USA;3. Department of Basic Medical Sciences, Tsinghua University School of Medicine, Beijing 100084, China
Abstract:The mismatch repair (MMR) family complexes Msh4-Msh5 and Mlh1-Mlh3 act with Exo1 and Sgs1-Top3-Rmi1 in a meiotic double strand break repair pathway that results in the asymmetric cleavage of double Holliday junctions (dHJ) to form crossovers. This review discusses how meiotic roles for Msh4-Msh5 and Mlh1-Mlh3 do not fit paradigms established for post-replicative MMR. We also outline models used to explain how these factors promote the formation of meiotic crossovers required for the accurate segregation of chromosome homologs during the Meiosis I division.
Keywords:Meiosis  Crossing over  Msh4-Msh5  Mlh1-Mlh3  Holliday junction resolution
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