The mechanism by which these SOS genes are specifically transcribed when the cell experiences DNA damage is through relief of LexA repression. This de-repression TGR5 occurs after RecA binds ssDNA, an indicator of DNA damage, and induces LexA self-cleavage. The normal state of repression in the absence of DNA damage thus prevents constitutive production of the entire SOS regulon, and SOS mutagenesis. This general model of SOS gene induction and function, which has been developed to a significant extent in Escherichia coli, is conserved throughout proteobacterial classes, albeit imperfectly. Further components of the SOS model of gene regulation are absent in Acinetobacter species of this order. None of its fellow members of the family Moraxellaceae possess umuD homologs, which may have implications for the ability of these organisms to undergo SOS mutagenesis after DNA damage. Additionally, no lexA homolog has been identified in this genus. Nevertheless, in the non-pathogenic genetic model organism Acinetobacter baylyi ADP1, previous investigations of the DNA damage response demonstrated that two genes are induced by mitomycin C and UV exposure in this strain. These two induced genes are recA, and ddrR, a gene of unknown function found only in the genus Acinetobacter. ddrR is transcribed divergently from umuDAb, which is itself an unusual component of the DNA damage response of this species. UmuDAb is a UmuD homolog that is required for full induction of ddrR, but it is not known whether ADP1 uses it to induce other genes that are, in other bacteria, part of the SOS response. UmuDAb carries out Caffeic Acid Phenethyl Ester self-cleavage in a RecA-dependent manner after cells experience diverse forms of DNA damage, and thus shares features with both the DNA polymerase V component UmuD and the LexA repressor. Recent work demonstrates that in A. baumannii ATCC 17978, UmuDAb binds to and represses the promoters of umuDC homologs and so might serve as a LexA analog for this genus. Multiple umuD and umuC homologs co-exist in A. baumannii strains, and at least some of these strains display DNA damage-induced mutagenesis.