Can catalyze the hydrolysis of ATP in the presence of single-stranded DNA, the ATP-dependent uptake of single-stranded DNA by duplex DNA, and the ATP-dependent hybridization of homologous single-stranded DNAs. It interacts with LexA causing its activation and leading to its autocatalytic cleavage (By similarity). Probably involved in base excision repair (PubMed:19303848). Following severe irradiation (7 kGy of gamma irradiation) genomic DNA is fragmented. DNA is progressively degraded for the first 1.5 hours after IR, in a step promoted by RecA and counterbalanced by DNA Pol I and Pol III, followed by massive DNA synthesis and genome reassembly in the next hour. Optimal priming of DNA synthesis requires both RecA and RadA, Pol III initiates DNA synthesis while both Pol I and Pol III are required for its contination. In the absence of RecA the majority of the chromosome is still reconstituted, via either single-strand annealing or non-homologous end joining (PubMed:19303848). Reduced DNA synthesis rate even in the absence of ionizing radiation (IR) (PubMed:19303848). Cells lacking this gene have a reduced capacity to survive IR (from 90% survival to <10(-7)), DNA repair following IR is slow (PubMed:20451472, PubMed:19303848). Single recA mutants rarely reconstitutes the whole genome following IR, and their DNA is not degraded post-IR (PubMed:19303848). A double recA-ddrB disruption shows no signs of DNA repair 24 hours after IR (PubMed:20451472). Double recA-radA deletion mutants have a more severe effect than either mutation alone after IR (PubMed:19303848). Belongs to the RecA family.