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Seguela-Arnaud, M.

Publications and source records attributed to Seguela-Arnaud, M..

3 recordsLinked to original sources

Unleashing meiotic crossovers in hybrid plants

Meiotic crossovers shuffle parental genetic information, providing novel combinations of alleles on which natural or artificial selection can act. However, crossover events are relatively rare, typically one to three exchange points per chromosome pair. Recent work has identified three pathways limiting meiotic crossovers in Arabidopsis thaliana, that rely on the activity of FANCM1, RECQ42 and FIGL13, respectively. Here, we analyzed recombination in plants where one, two or three of these pathways were disrupted, in both pure line and hybrid contexts. The highest effect was observed when combining recq4 and figl1 mutations, which increased the hybrid genetic map length from 389 to 3037 centiMorgans. This corresponds to an unprecedented 7.8-fold increase in crossover frequency. Disrupting the three pathways do not further increases recombination, suggesting that some upper limit has been reached. The increase in crossovers is not uniform along chromosomes and rises from centromere to telomere. Finally, while in wild type recombination is much higher in male than in female meiosis (490 cM vs 290 cM), female recombination is higher than male in recq4 figl1 (3200 cM vs 2720 cM), suggesting that the factors that make wild-type female meiosis less recombinogenic than male wild-type meiosis do not apply in the mutant context. The massive increase of recombination observed in recq4 figl1 hybrids opens the possibility to manipulate recombination to enhance plant breeding efficiency.

genetics

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

Homologous recombination is central to repair DNA double-strand breaks (DSB), 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 CO formation remain elusive. Here, we identified through protein-protein interaction and genetic 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 stand exchange step of homologous recombination. Arabidopsis flip mutants recapitulates the figl1 phenotype, with enhanced meiotic recombination associated with change in DMC1 dynamics. Our data thus suggest that FLIP and FIGL1 form a conserved complex that regulates the crucial step of strand invasion in homologous recombination.

genetics

Massive crossover elevation via combination of HEI10 and recq4a recq4b during Arabidopsis meiosis

During meiosis homologous chromosomes undergo reciprocal crossovers, which generate genetic diversity and underpin classical crop improvement. Meiotic recombination initiates from DNA double strand breaks, which are processed into single-stranded DNA that can invade a homologous chromosome. The resulting joint molecules can ultimately be resolved as crossovers. In Arabidopsis, competing pathways balance the repair of [~]100-200 meiotic DSBs into [~]10 crossovers per meiosis, with the excess DSBs repaired as non-crossovers. In order to bias DSB repair towards crossovers, we simultaneously increased dosage of the pro-crossover E3 ligase gene HEI10 and introduced mutations in the anti-crossover helicase genes RECQ4A and RECQ4B. As HEI10 and recq4a recq4b increase interfering and non-interfering crossover pathways respectively, they combine additively to yield a massive meiotic recombination increase. Interestingly, we also show that increased HEI10 dosage increases crossover coincidence, which indicates an effect of HEI10 on interference. We also show that patterns of interhomolog polymorphism and heterochromatin drive recombination increases towards the sub-telomeres in both HEI10 and recq4a recq4b backgrounds, while the centromeres remain crossover-suppressed. These results provide a genetic framework for engineering meiotic recombination landscapes in plant genomes.

genetics