Journal
NUCLEIC ACIDS RESEARCH
Volume 48, Issue 15, Pages 8474-8489Publisher
OXFORD UNIV PRESS
DOI: 10.1093/nar/gkaa587
Keywords
-
Categories
Funding
- Academia Sinica, Taiwan [AS-105-TP-B07, AS108-TP-B07]
- Ministry of Science and Technology, Taiwan, Republic of China [MOST163-2311-B-001-016-MY3]
- MOST
- Academia Sinica [AS108-TP-B07]
Ask authors/readers for more resources
Highly toxic DNA double-strand breaks (DSBs) readily trigger the DNA damage response (DDR) in cells, which delays cell cycle progression to ensure proper DSB repair. In Saccharomyces cerevisiae, mitotic S phase (20-30 min) is lengthened upon DNA damage. During meiosis, Spo11-induced DSB onset and repair lasts up to 5 h. We report that the NH2-terminal domain (NTD; residues 1-66) of Rad51 has dual functions for repairing DSBs during vegetative growth and meiosis. Firstly, Rad51-NTD exhibits autonomous expression-enhancing activity for high-level production of native Rad51 and when fused to exogenous beta-galactosidase in vivo. Secondly, Rad51-NTD is an S/T-Q cluster domain (SCD) harboring three putative Mec1/Tel1 target sites. Mec1/Tel1-dependent phosphorylation antagonizes the proteasomal degradation pathway, increasing the half-life of Rad51 from similar to 30 min to >= 180 min. Our results evidence a direct link between homologous recombination and DDR modulated by Rad51 homeostasis.
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