Abstract: LexA and RecA play a crucial role in SOS response in Escherichia coli. In classical SOS response, LexA functions as a repressor to regulate the expression of many genes including RecA after DNA damage occurs. Previous studies showed that LexA1 or LexA2 is not involved in RecA induction in Deinococcus radiodurans. In this study, we constructed a double mutant of lexA1 and lexA2. Results showed that mutation of lexAl and lexA2 resulted in an apparent decrease in growth rate and an increased resistance to ultraviolet and hydrogen peroxide compared with wild type R1 and two single mutants. However, this double mutant did not exhibit any remarkably increased constitutive expression of RecA under normal conditions, just like wild type R1 and two single mutants, suggesting that neither LexA1 nor LexA2 is involved in the induced expression of RecA. Further transcriptional assay showed that LexA1 and LexA2 together participated in many regulatory pathways involved in cell division, protein synthesis, antioxidant process, transcription regulation and other mechanisms. These results indicate that there should be a new mechanism by which these damage-induced proteins are regulated in D. radiodurans.