RecAdependent

RecA-dependent refers to cellular processes in bacteria that require the RecA recombinase to function. RecA is a central enzyme in homologous recombination and DNA damage tolerance, capable of forming nucleoprotein filaments on single-stranded DNA and promoting strand exchange with a homologous duplex. This activity underpins accurate repair of damaged DNA and genetic recombination.

RecA-dependent pathways rely on loading proteins such as RecBCD or RecFOR to establish RecA filaments at DNA ends or gaps. Once loaded, RecA facilitates homologous pairing and strand invasion, enabling repair of double-strand breaks, stalled replication forks, and post-replication gaps. Depending on the context, this can lead to gene conversion or, in some cases, crossover events, contributing to genetic diversity or genome stability.

A major RecA-dependent process is the bacterial SOS response, a coordinated transcriptional program triggered by extensive DNA damage. Activated RecA (RecA*) stimulates autocleavage of the LexA repressor, derepressing SOS genes that encode DNA repair enzymes, specialized polymerases, and cell-cycle modulators. This response enhances survival under genotoxic stress but can increase mutagenesis.

RecA is also involved in replication restart through recombination-mediated mechanisms that help restart stalled forks, preserving chromosome integrity. While many DNA repair and recombination processes are RecA-dependent, some pathways can operate without RecA, albeit typically less efficiently or with different fidelity. In eukaryotes, the functional counterpart is Rad51, illustrating the conserved importance of RecA-like proteins in maintaining genome integrity.