DNA-dependent ATPase involved in processing of recombination intermediates, plays a role in repairing DNA breaks. Stimulates the branch migration of RecA-mediated strand transfer reactions, allowing the 3' invading strand to extend heteroduplex DNA faster. Binds ssDNA in the presence of ADP but not other nucleotides, has ATPase activity that is stimulated by ssDNA and various branched DNA structures, but inhibited by SSB. Does not have RecA's homology-searching function. Plays a role in DNA damage repair (Ref.2). Following severe irradiation (IR, 7 kGy of gamma irradiation), genomic DNA is fragmented and 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. This is 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 continuation (PubMed:19303848). Has a putative N-terminal zinc-finger, a middle region with homology to RecA with ATPase motifs including the RadA KNRFG motif, while the C-terminus is homologous to Lon protease (By similarity). Absence of the zinc-finger domain gives a slight increase in sensitivity to gamma and UV irradiation, absence of the Lon protease domain gives slightly increased resistance to gamma and UV irradiation. Moderately decreased resistance to gamma and UV irradiation, no effect on H(2)O(2) resistance (Ref.2). Slightly reduced DNA synthesis rate even in the absence of ionizing radiation (IR); after IR chromosome fragment assembly is delayed. Double recA-radA deletion mutants have lower rates of DNA synthesis than the recA deletion alone with or without IR (PubMed:19303848). Belongs to the RecA family. RadA subfamily.