相同組換えの制御メカニズムの解明と人工的コントロール方法の開発
Type: report
Abstract: Homologous recombination (HR) is essential mechanism to maintain genome stability. Homology search and strand invasion steps in HR are catalyzed by RAD51 protein. Formation of RAD51 filament on ssDNA is necessary to execute proper HR and restart of DNA replication forks, while inappropriate RAD51 filament formation causes genome instability. Hence, RAD51 filament formation is tightly suppressed by anti-recombinases, which promote the dissociation of RAD51. However, the mechanisms underlying genome instability caused by inappropriate RAD51 assembly and the suppression by anti-recombinases remain largely unknown. Here, we report a role for the human AAA+ ATPase, FIGNL1 as a novel anti-recombinase. FIGNL1-deficient cells show the excessive RAD51 recruitment. RAD51 filaments persist and cause defects in chromosome segregation. Our data suggest that recombination intermediates caused by inappropriate RAD51 assembly prevent chromosome segregation and induce genome instability.
Author: Matsuzaki, Kenichiro
Institution: Kindai University
Language: Japanese
Topic: DNA Repair Mechanisms
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W7146464250