Alkylating agents are widespread in the environment and also occur endogenously. 
They can be cytotoxic or mutagenic to the cells introducing alkylated bases to 
DNA or RNA. All organisms have evolved multiple DNA repair mechanisms to 
counteract the effects of DNA alkylation: the most cytotoxic lesion, 
N(3)-methyladenine (3meA), is excised by AlkA glycosylase initiating base 
excision repair (BER); toxic N(1)-methyladenine (1meA) and N(3)-methylcytosine 
(3meC), induced in DNA and RNA, are removed by AlkB dioxygenase; and mutagenic 
and cytotoxic O(6)-methylguanine (O(6) meG) is repaired by Ada 
methyltransferase. In Escherichia coli, Ada response involves the expression of 
four genes, ada, alkA, alkB, and aidB, encoding respective proteins Ada, AlkA, 
AlkB, and AidB. The Ada response is conserved among many bacterial species; 
however, it can be organized differently, with diverse substrate specificity of 
the particular proteins. Here, an overview of the organization of the Ada 
regulon and function of individual proteins is presented. We put special effort 
into the characterization of AlkB dioxygenases, their substrate specificity, and 
function in the repair of alkylation lesions in DNA/RNA.