Toxic component of a type II toxin-antitoxin (TA) system. Has RNase activity and preferentially cleaves at the 3'-end of purine ribonucleotides (By similarity). Overexpression in M.tuberculosis or M.smegmatis inhibits colony formation in a bacteriostatic rather than bacteriocidal fashion. Its toxic effect is neutralized by coexpression with cognate antitoxin RelB2 (shown only for M.smegmatis). Overexpression also increases the number of gentamicin-tolerant and levofloxacin-tolerant persister cells. In combination with cognate antitoxin RelF represses its own promoter. Has been seen to bind DNA in complex with antitoxin RelF but not alone. Interacts with cognate antitoxin RelF, which neutralizes the toxin. Also interacts with non-cognate antitoxin RelB in vitro, in M.smegmatis this neutralizes the toxicity of this toxin. Expressed in log phase cells. Induced by treatment with rifampicin and gentamicin as well as by oxidative, nitrosative and nutritional stress. Induced in the lungs of mice infected for 4 weeks. A member of the relFG operon. No visible phenotype in culture or upon infection of mice. Significantly fewer persister cells are generated in vitro following exposure to rifampicin and gentamicin, but in infected mice no differences are seen. Belongs to the RelE toxin family.