Cyclic di-AMP regulates genome stability and drug resistance in <i>Mycobacterium</i> through RecA-dependent and RecA-independent recombination.

ABSTRACT: In Escherichia coli, RecA plays a central role in the rescue of stalled replication forks, double-strand break (DSB) repair, homologous recombination (HR), and induction of the SOS response. While the RecA-dependent pathway is dominant, alternative HR pathways that function independently of RecA do exist, but relatively little is known about the underlying mechanism. Several studies have documented that a variety of proteins act as either positive or negative regulators of RecA to ensure high-fidelity HR and genomic stability. Along these lines, we previously demonstrated that the second messenger cyclic di-AMP (c-di-AMP) binds to mycobacterial RecA proteins, but not to E. coli RecA, and inhibits its DNA strand exchange activity in vitro via the disassembly of RecA nucleoprot

SUBMITTER: Mudgal S 

PROVIDER: S-EPMC11653572 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature