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 antitoxin RelJ (shown only for M.smegmatis). Overexpression also increases the number of rifampcin-tolerant persister cells. In combination with RelJ represses its own promoter. Several DNA-protein complexes are formed in vitro depending on the RelJ:RelK ratio. Forms a toxin-antitoxin complex with RelJ, perhaps RelJ(2)-RelK, in which the toxin is probably inactive. Also interacts with antitoxins RelB and RelF in vitro, in M.smegmatis coexpression with non-cognate antitoxin RelB increases the toxicity of RelK while little change is seen in the RelFK pair. Expressed in log phase cells. Induced by treatment with rifampicin and gentamicin as well as by nitrosative and oxidative stress. Expressed in human macrophages 110 hours after infection. Induced in the lungs of mice infected for 4 weeks. A member of the relJK operon. No visible phenotype in culture or upon infection of mice. Significantly fewer persister cells are generated following exposure to gentamicin, levofloxacin and isoniazid. Belongs to the YoeB family.