Journal
MOLECULAR CELL
Volume 37, Issue 2, Pages 259-272Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2009.12.026
Keywords
-
Categories
Funding
- Fratelli Confalonied and Cariplo Foundations
- AIRC
- MIUR
- Fondazione Cariplo
- European Union
- Cancer Research UK
- BBSRC
- BBSRC [BB/D020336/2] Funding Source: UKRI
- MRC [MC_U120097113] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/D020336/2] Funding Source: researchfish
- Medical Research Council [MC_U120097113] Funding Source: researchfish
Ask authors/readers for more resources
Homologous recombination (HR) is essential for repair of meiotic DNA double-strand breaks (DSBs). Although the mechanisms of RAD-51-DNA filament assembly and strand exchange are well characterized, the subsequent steps of HR are less well defined. Here, we describe a synthetic lethal interaction between the C. elegans helicase helq-1 and RAD-51 paralog rfs-1, which results in a block to meiotic DSB repair after strand invasion. Whereas RAD-51-ssDNA filaments assemble at meiotic DSBs with normal kinetics in helq-1, rfs-1 double mutants, persistence of RAD-51 foci and genetic interactions with rtel-1 suggest a failure to disassemble RAD-51 from strand invasion intermediates. Indeed, purified HELQ-1 and RFS-1 independently bind to and promote the disassembly of RAD-51 from double-stranded, but not single-stranded, DNA filaments via distinct mechanisms in vitro. These results indicate that two compensating activities are required to promote postsynaptic RAD-51 filament disassembly, which are collectively essential for completion of meiotic DSB repair.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available