When E. coli cells are treated with sublethal levels of alkylating agents, they become more resistant to the lethal and mutagenic effects of subsequent high-level treatments with alkylating agents.  This increased resistance has been called the adaptive response to alkylating agents.  It is the result of the induction of genes that increase the cell's capacity to repair alkylation lesions in DNA.  We have initiated a genetic study designed to learn what genes are induced by alkylation treatments, how they are regulated and what are the functions of their products.  To date five genes or operons have been identified that are induced by alkylation treatments.  They were identified as fusions of the lac operon to promoters that caused increased Beta-galactosidase activity upon alkylation treatment.  Of these lac fusions, two are linked to promoters of genes known to be involved in the repair of alkylation damage.  The aidA (alkylation inducible) gene codes for the alkA gene product and aidD is a fusion to the promoter of the ada/alkB operon.  aidB, aidC and aidI represent fusions to genes that had not been previously identified.  Studies of the regulation of these aid genes shows that aidA, aidB and aidD fall into one regulatory group and are controlled by the ada gene, a regulatory element needed for normal expression of the adaptive response.  aidC and aidI each appear to be regulated separately and are not under ada control.  Moreover, aidC is induced by MNNG but not by MMS, whereas aidI is induced by MMS but not by MNNG.  Therefore, these two genes must respond to different induction signals.