Toxic component of a hybrid type II/IV toxin-antitoxin (TA) system. Its toxic effect is neutralized by cognate antitoxin DarG (PubMed:27939941). ADP-ribosylates ssDNA, preferentially in the motif TTTW. Uncontrolled expression of DarT leads to ADP-ribosylation of the origin of chromosomal replication DNA in cells (in vitro the most heavily modified motifs are TTTT/A in the OriC lower strand) and growth arrest (PubMed:34408320). Is very toxic to E.coli, it cannot be expressed in E.coli (PubMed:27939941). Experiments in situ in which antitoxin DarG levels are depleted (similar to overexpression of DarT) lead to cell death; expression of wild-type DarG protein from M.tuberculosis or T.aquaticus restores growth. Cells with decreased levels of DarG are more sensitive to bedaquilline (targets respiration), DNA-damaging drugs (mitomycin C, netropsin) and transcription-targeted drugs (rifabutin and rifampicin). When DarG is depleted, a DNA-damage response is induced and mutability is increased, suggesting ADP-ribosylation of DNA is the toxic effect (PubMed:32634279). a thymidine in DNA + NAD(+) = an N-(ADP-alpha-D-ribosyl)-thymidine in DNA + H(+) + nicotinamide Forms a complex with cognate antitoxin DarG; this complex neutralizes the toxic effect of DarT. Part of the dnaB-darT-darG operon. The NAD(+)-binding element stabilizes the ADP-ribosylating turn-turn (ARTT) loop which confers substrate specificity; both domains contribute to ssDNA-binding. A double darT-darG deletion shows no change in growth in culture, upon infection of mice or upon exposure to a variety of stresses (PubMed:32634279). Another group finds the double knockout gives a competitive advantage over wild-type cells in liquid culture growth experiments (PubMed:34408320). Belongs to the DarT ADP-ribosyltransferase family.