作者: Richa Gupta , Daniel Barkan , Gil Redelman-Sidi , Stewart Shuman , Michael S. Glickman
DOI: 10.1111/J.1365-2958.2010.07463.X
关键词:
摘要: Bacterial pathogens rely on their DNA repair pathways to resist genomic damage inflicted by the host. double-strand breaks (DSBs) are especially threatening bacterial viability. DSB homologous recombination (HR) requires nucleases that resect ends and a strand exchange protein facilitates homology search. RecBCD RecA perform these functions in Escherichia coli constitute major pathway of error-free repair. Mycobacteria, including human pathogen M. tuberculosis, elaborate an additional error-prone via non-homologous end-joining (NHEJ) catalysed Ku ligase D (LigD). Little is known about relative contributions HR NHEJ mycobacterial chromosome repair, factors dictate choice, or existence pathways. Here we demonstrate Mycobacterium smegmatis has three options: HR, novel mechanism single-strand annealing (SSA). Inactivation SSA compensated elevated HR. We find does not participate confer resistance ionizing radiation (IR), but required for RecA-independent pathway. In contrast, helicase-nuclease AdnAB participates RecA-dependent pathway, determinant IR oxidative damage. These findings reveal distinctive features most notably dedication machines distinct