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• W2953114902 endingPage "e1007317" @default.
• W2953114902 startingPage "e1007317" @default.
• W2953114902 abstract "Homologous recombination is central to repair DNA double-strand breaks, either accidently arising in mitotic cells or in a programed manner at meiosis. Crossovers resulting from the repair of meiotic breaks are essential for proper chromosome segregation and increase genetic diversity of the progeny. However, mechanisms regulating crossover formation remain elusive. Here, we identified through genetic and protein-protein interaction screens FIDGETIN-LIKE-1 INTERACTING PROTEIN (FLIP) as a new partner of the previously characterized anti-crossover factor FIDGETIN-LIKE-1 (FIGL1) in Arabidopsis thaliana. We showed that FLIP limits meiotic crossover together with FIGL1. Further, FLIP and FIGL1 form a protein complex conserved from Arabidopsis to human. FIGL1 interacts with the recombinases RAD51 and DMC1, the enzymes that catalyze the DNA strand exchange step of homologous recombination. Arabidopsis flip mutants recapitulate the figl1 phenotype, with enhanced meiotic recombination associated with change in counts of DMC1 and RAD51 foci. Our data thus suggests that FLIP and FIGL1 form a conserved complex that regulates the crucial step of strand invasion in homologous recombination." @default.
• W2953114902 created "2019-06-27" @default.
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• W2953114902 date "2018-04-02" @default.
• W2953114902 modified "2023-10-18" @default.
• W2953114902 title "FIGL1 and its novel partner FLIP form a conserved complex that regulates homologous recombination" @default.
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• W2953114902 doi "https://doi.org/10.1371/journal.pgen.1007317" @default.
• W2953114902 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5897033" @default.
• W2953114902 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29608566" @default.
• W2953114902 hasPublicationYear "2018" @default.
• W2953114902 type Work @default.
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