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PLoS Genet. 2018 Apr 2;14(4):e1007317. doi: 10.1371/journal.pgen.1007317. eCollection 2018 Apr.

FIGL1 and its novel partner FLIP form a conserved complex that regulates homologous recombination.

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Institut Jean-Pierre Bourgin, UMR1318 INRA-AgroParisTech, Université Paris-Saclay, RD10,Versailles, France.
Université Paris-Sud, Université Paris-Saclay, Orsay, France.
Department of Plant Biotechnology and Bioinformatics, Ghent University, Ghent, Belgium.
VIB Center for Plant Systems Biology, Ghent, Belgium.
Department of Biochemistry, Ghent University, Ghent, Belgium.
VIB Center for Medical Biotechnology, Ghent, Belgium.
Institute for Integrative Biology of the Cell (I2BC), Commissariat à l'Energie Atomique et aux Energies Alternatives (CEA), Centre National de la Recherche Scientifique (CNRS), Université Paris-Sud, CEA-Saclay, Gif-sur-Yvette, France.


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.

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