title: Sufficient amounts of functional HOP2/MND1 complex promote interhomolog DNA repair but are dispensable for intersister DNA repair during meiosis in Arabidopsis.
abstract: During meiosis, homologous recombination (HR) is essential to repair programmed DNA double-strand breaks (DSBs), and a dedicated protein machinery ensures that the homologous chromosome is favored over the nearby sister chromatid as a repair template. The homologous-pairing protein2/meiotic nuclear division protein1 (HOP2/MND1) protein complex has been identified as a crucial factor of meiotic HR in Arabidopsis thaliana, since loss of either MND1 or HOP2 results in failure of DNA repair. We isolated two mutant alleles of HOP2 (hop2-2 and hop2-3) that retained the capacity to repair meiotic DSBs via the sister chromatid but failed to use the homologous chromosome. We show that in these alleles, the recombinases radiation sensitive51 (RAD51) and disrupted meiotic cDNA1 (DMC1) are loaded, but only the intersister DNA repair pathway is activated. The hop2-2 phenotype is correlated with a decrease in HOP2/MND1 complex abundance. In hop2-3, a truncated HOP2 protein is produced that retains its ability to bind to DMC1 and DNA but forms less stable complexes with MND1 and fails to efficiently stimulate DMC1-driven D-loop formation. Genetic analyses demonstrated that in the absence of DMC1, HOP2/MND1 is dispensable for RAD51-mediated intersister DNA repair, while in the presence of DMC1, a minimal amount of functional HOP2/MND1 is essential to drive intersister DNA repair.
authors.affiliation: Department of Chromosome Biology, Max F. Perutz Laboratories, University of Viena, A-1030 Viena, Austria.
authors.forename: Clemens
authors.initials: C
authors.lastname: Uanschou
authors.forename: Arnaud
authors.initials: A
authors.lastname: Ronceret
authors.forename: Mona
authors.initials: M
authors.lastname: Von Harder
authors.forename: Arnaud
authors.initials: A
authors.lastname: De Muyt
authors.forename: Daniel
authors.initials: D
authors.lastname: Vezon
authors.forename: Lucie
authors.initials: L
authors.lastname: Pereira
authors.forename: Liudmila
authors.initials: L
authors.lastname: Chelysheva
authors.forename: Wataru
authors.initials: W
authors.lastname: Kobayashi
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Kurumizaka
authors.forename: Peter
authors.initials: P
authors.lastname: Schlögelhofer
authors.forename: Mathilde
authors.initials: M
authors.lastname: Grelon
mesh_terms: D017360:Arabidopsis / Q000166:cytology* / Q000235:genetics / Q000378:metabolism; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D002842:Chromatids / Q000235:genetics / Q000378:metabolism; D053903:DNA Breaks, Double-Stranded; D004260:DNA Repair; D008540:Meiosis / Q000235:genetics*; D008957:Models, Genetic; D009154:Mutation; D010770:Phosphotransferases / Q000378:metabolism / Q000502:physiology*; D055550:Protein Stability; D011938:Rec A Recombinases / Q000235:genetics / Q000378:metabolism / Q000502:physiology
chemical_list: C117967:AHP2 protein, Arabidopsis; D029681:Arabidopsis Proteins; D018797:Cell Cycle Proteins; C514180:MND1 protein, Arabidopsis; D010770:Phosphotransferases; C513034:ATDMC1 protein, Arabidopsis; D011938:Rec A Recombinases