Toxic component of a type I toxin-antitoxin (TA) system; expression in the absence of cognate antisense antitoxin SR4 RNA leads to cell lysis (PubMed:22229825, PubMed:23969414). Induced expression causes membrane invaginations that dislocate the cell wall synthesis machinery, leading to eventual death. Unlike many type I TA systems it does not form pores (PubMed:26234942). Base pairing occurs between the 3' UTRs of bsrG mRNA and SR4 RNA, which leads to initiation of degradation by RNase III (rnc) followed by the action of RNase Y (rny) and RNase R (rnr). Not toxic when expressed in E.coli (PubMed:22229825, PubMed:23969414). When induced during logarithmic growth it only slowly exerts its toxic effect. Expression during log growth leads to significant disturbances of cell envelope biosynthesis and cell morphology, causing cell membrane invaginations and delocalization of cell division and cell wall synthesis machinery. Cell lysis depends on mreB, lytC and lytD, suggesting expression of bsrG triggers autolysis rather than disintegration of the membrane. Additionally expression of bsrG also inhibits transcription (PubMed:26234942). Fusion of GFP to the C-terminus renders the protein non-toxic but still able to associate with the membrane. Accumulates by 4 hours post-innoculation and into stationary phase in rich media; maximum expression occurs at 6 hours (PubMed:18948176). Low expression early in rich and minimal medium, higher expression after. The antitoxin antisense RNA SR4 is constitutively expressed at a constant level in all growth conditions and media tested. bsrG mRNA levels decrease rapidly upon 48 degrees Celsius heat shock (PubMed:22229825, PubMed:26802042). SR4 RNA not only base pairs with bsrG mRNA promoting its degradation, but also inhibits its translation as it sequesters the Shine-Dalgarno sequence (PubMed:23969414). Non-essential, it can be deleted. The gene for the antisense antitoxin SR4 RNA cannot be deleted. Encoded in the SPbeta prophage; retention of this TA system may prevent the bacterium from losing SPbeta from its genome.