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

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...

Full description

Saved in:
Bibliographic Details
Published in:PLoS genetics 2018-04, Vol.14 (4), p.e1007317
Main Authors: Fernandes, Joiselle Blanche, Duhamel, Marine, Seguéla-Arnaud, Mathilde, Froger, Nicole, Girard, Chloé, Choinard, Sandrine, Solier, Victor, De Winne, Nancy, De Jaeger, Geert, Gevaert, Kris, Andrey, Philippe, Grelon, Mathilde, Guerois, Raphael, Kumar, Rajeev, Mercier, Raphaël
Format: Article
Language:English
Subjects:
Arabidopsis
Arabidopsis thaliana
Bioinformatics
Biology
Biology and Life Sciences
Biotechnology
Cancer
Chromosomes
Computer and Information Sciences
Deoxyribonucleic acid
DNA
DNA damage
DNA repair
Genetic aspects
Genetic crosses
Genetic diversity
Genetic recombination
Homologous recombination
Life Sciences
Meiosis
Observations
Phenotypes
Protein interaction
Protein-protein interactions
Proteins
Research and Analysis Methods
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:1553-7404
1553-7390
1553-7404
DOI:10.1371/journal.pgen.1007317