Toxic component of a hybrid type II/IV toxin-antitoxin (TA) system. ADP-ribosylates ssDNA in the sequence TTT/TCT. Its toxic effect is neutralized by cognate antitoxin DarG (PubMed:32023456). May target ssDNA loops during DNA replication, probably modifies thymidine (Probable). Wild-type protein cannot be expressed at low levels in the absence of its cognate antitoxin, but a mutant protein (G49D) can be expressed, which slows growth, rapidly inhibits DNA replication, and induces RecA expression and the SOS response (PubMed:32023456). The slow growth phenotype can be suppressed by cognate antitoxin DarG. Has no activity on dsDNA in vitro (PubMed:32023456). In vivo ADP-ribosylates genomic DNA (gDNA) (PubMed:34408320). Genetic data strongly suggests ADP-ribosylation by DarT probably generates ssDNA gaps that are repaired by the RecFOR-mediated homologous recombination pathway (RuvAB, RecG) and resolved by RuvC. In some cases these gaps probably migrate into dsDNA, where they are resolved by nucleotide excision repair (NER) detected by UvrAB, excised by UvrC, removed by UvrD, and repaired by Pol I and ligase. Other pathways may also be involved in ADP-ribosylation removal from DNA (Probable). a thymidine in DNA + NAD(+) = an N-(ADP-alpha-D-ribosyl)-thymidine in DNA + H(+) + nicotinamide Interacts with DarG, primarily via the C-terminus of DarG (tested with DarT mutant G49D), which probably sequesters DarT and inhibits it. The NAD(+)-binding element stabilizes the ADP-ribosylating turn-turn (ARTT) loop which confers substrate specificity; both domains contribute to ssDNA-binding. Belongs to the DarT ADP-ribosyltransferase family.