HslO ameliorates arrested ΔrecA polA cell growth and reduces DNA damage and oxidative stress responses.

ABSTRACT: Chromosome damage combined with defective recombinase activity has been widely considered to render cells inviable, owing to deficient double-strand break repair. However, temperature-sensitive recAts polA cells grow well upon induction of DNA damage and supplementation with catalase at restrictive temperatures. These treatments reduce intracellular reactive oxygen species (ROS) levels, which suggests that recAts polA cells are susceptible to ROS, but not chronic chromosome damage. Therefore, we investigated whether polA cells can tolerate a complete lack of recombinase function. We introduced a ΔrecA allele in polA cells in the presence or absence of the hslO-encoding redox molecular chaperon Hsp33 expression plasmid. Induction of the hslO gene with IPTG resulted in increased cell viabili

SUBMITTER: Kaidow A 

PROVIDER: S-EPMC9789031 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature