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

被引：84

作者：

Fernandes, Joiselle Blanche ^{[1
,2
]}

Duhamel, Marine ^{[1
]}

Seguela-Arnaud, Mathilde ^{[1
]}

Froger, Nicole ^{[1
]}

Girard, Chloe ^{[1
]}

Choinard, Sandrine ^{[1
]}

Solier, Victor ^{[1
]}

De Winne, Nancy ^{[3
,4
]}

De Jaeger, Geert ^{[3
,4
]}

Gevaert, Kris ^{[5
,6
]}

Andrey, Philippe ^{[1
]}

Grelon, Mathilde ^{[1
]}

Guerois, Raphael ^{[7
]}

Kumar, Rajeev ^{[1
]}

Mercier, Raphael ^{[1
]}

机构：

[1] Univ Paris Saclay, INRA AgroParisTech, Inst Jean Pierre Bourgin, UMR1318, RD10, Versailles, France

[2] Univ Paris Saclay, Univ Paris Sud, Orsay, France

[3] Univ Ghent, Dept Plant Biotechnol & Bioinformat, Ghent, Belgium

[4] VIB, Ctr Plant Syst Biol, Ghent, Belgium

[5] Univ Ghent, Dept Biochem, Ghent, Belgium

[6] VIB, Ctr Med Biotechnol, Ghent, Belgium

[7] Univ Paris Sud, Commissariat Energie Atom & Energies Alternat CEA, Inst Integrat Biol Cell I2BC, CEA Saclay,CNRS, Gif Sur Yvette, France

来源：

PLOS GENETICS | 2018年 / 14卷 / 04期

基金：

欧洲研究理事会;

关键词：

STRAND BREAK FORMATION; MEIOTIC RECOMBINATION; CROSSOVER INTERFERENCE; CHROMOSOME SYNAPSIS; PROTEIN-SEQUENCE; ARABIDOPSIS; MEIOSIS; ENDONUCLEASE; HELICASE; SGS1;

D O I：

10.1371/journal.pgen.1007317

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

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.

引用

页数：22

共 71 条

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