Antitoxin component of a type II toxin-antitoxin (TA) system. Upon overexpression neutralizes the effect of overexpressed cognate toxin VapC. Overexpression alone prevents cells from entering a nonculturable dormant state, probably as it binds endogenous VapC (PubMed:24417293). The TA system acts as a post-transcriptional regulator of carbon metabolism; in M.smegmatis 3 TA systems (VapB-VapC, MazE-MazF and Phd-Doc) may be involved in monitoring the nutritional supply and physiological state of the cell, linking catabolic with anabolic reactions. Translation of vapC mRNA requires VapB. Forms a complex with cognate toxin VapC. Expression is low but constitutive, and repressed by VapB-VapC. Member of the vapB-vapC operon. The vapB-vapC operon is not essential; cells grow faster than wild-type on rich and minimal glycerol-containing medium. The operon deletion mutants die faster than wild-type under potassium-limiting conditions, which is prevented by overexpression of vapB (PubMed:24417293). The vapB antitoxin gene can be disrupted without causing death, however despite elevated vapC transcription, no VapC protein could be detected, suggesting that RNA processing and translational coupling are important in VapC expression. A triple TA mutant (missing vapB-vapC, mazE-mazF and phd-doc TA systems) survives antibiotic challenge, suggesting the TA systems are not required to generate drug-resistant cells. However the triple mutant is more sensitive to oxidative and heat stress, and does not survive long term starvation during aerobic growth on complex medium. There is a difference in the level of branched-chain amino acids, which may play a role in monitoring the nutritional supply and physiological state of the cell.