Toxic component of a type II toxin-antitoxin (TA) system. A probable translation-dependent mRNA interferase. Overexpression causes cessation of cell growth and inhibits cell proliferation via inhibition of translation; this blockage is overcome by subsequent expression of antitoxin HigA. Overexpression causes cleavage of a number of mRNAs in a translation-dependent fashion, suggesting this is an mRNA interferase. Probably forms a complex with the antitoxin HigA which inhibits the mRNA interferase activity. Induced by amino acid starvation and when translation is blocked. Induction is decreased in the absence of the Lon protease suggesting, by homology to other toxin-antitoxin systems, that Lon may degrade the HigA antitoxin. Transcription is negatively regulated by the cognate locus, probably by HigA. A member of the higB-higA operon. Belongs to the HigB mRNA interferase family.