Toxic component of a type I toxin-antitoxin (TA) system; overexpression in the absence of cognate antisense antitoxin SR5 RNA leads to cell lysis (PubMed:26565032, PubMed:26940229). Base pairing occurs between the 3' UTRs of bsrE mRNA and SR5 RNA which leads to bsrE mRNA degradation initiated by RNase III (rnc) and RNase J1 (rnjA) (PubMed:26940229). Genetic evidence suggests an unidentified RNA-binding protein may exist that promotes TA RNA interaction (PubMed:26565032). Accumulates by 2 hours post-innoculation with maximal expression at 4 hours, and has disappeared by 8 hours in rich media (PubMed:18948176). Slightly different results were found in another study; in rich medium, expression increased slowly over time and was maximal at 6 hours. In minimal medium without glucose expression decreased as growth progressed, while in minimal medium plus glucose expression was constant during growth. SR5 antitoxin RNA is always present at levels equal to or in excess of toxin mRNA. Responds to a number of different stresses; ethanol, methanol and isopropanol and pH 9.1 stress cause a rapid loss of bsrE and SR5 mRNA, Fe(2+) limitation and pH 5.3 stress increases the SR5 RNA while oxygen depletion decreases SR5 with no effect on bsrE mRNA. Heat shock at 48 degrees Celsius causes a gradual decrease in bsrG mRNA (PubMed:26940229). Non-essential, it can be deleted on rich medium; the gene for the antisense antitoxin SR5 RNA can also be deleted without a visible phenotype. Encoded in the prophage-like P6 region.