FIGNL1 AAA+ ATPase remodels RAD51 and DMC1 filaments in pre-meiotic DNA replication and meiotic recombination

Masaru Ito (), Asako Furukohri, Kenichiro Matsuzaki, Yurika Fujita, Atsushi Toyoda and Akira Shinohara ()
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Masaru Ito: Osaka University, Suita
Asako Furukohri: Osaka University, Suita
Kenichiro Matsuzaki: Osaka University, Suita
Yurika Fujita: Osaka University, Suita
Atsushi Toyoda: National Institute of Genetics, Mishima
Akira Shinohara: Osaka University, Suita

Nature Communications, 2023, vol. 14, issue 1, 1-19

Abstract: Abstract The formation of RAD51/DMC1 filaments on single-stranded (ss)DNAs essential for homology search and strand exchange in DNA double-strand break (DSB) repair is tightly regulated. FIGNL1 AAA+++ ATPase controls RAD51-mediated recombination in human cells. However, its role in gametogenesis remains unsolved. Here, we characterized a germ line-specific conditional knockout (cKO) mouse of FIGNL1. Fignl1 cKO male mice showed defective chromosome synapsis and impaired meiotic DSB repair with the accumulation of RAD51/DMC1 on meiotic chromosomes, supporting a positive role of FIGNL1 in homologous recombination at a post-assembly stage of RAD51/DMC1 filaments. Fignl1 cKO spermatocytes also accumulate RAD51/DMC1 on chromosomes in pre-meiotic S-phase. These RAD51/DMC1 assemblies are independent of meiotic DSB formation. We also showed that purified FIGNL1 dismantles RAD51 filament on double-stranded (ds)DNA as well as ssDNA. These results suggest an additional role of FIGNL1 in limiting the non-productive assembly of RAD51/DMC1 on native dsDNAs during pre-meiotic S-phase and meiotic prophase I.

Date: 2023
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DOI: 10.1038/s41467-023-42576-w

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