Here we report mechanistic insights into bacterial death phase initiation that occurs as part of the bacterial life cycle. Porphyromonas gingivalis is a keystone pathogen in chronic periodontitis. A P. gingivalis mutant (ΔPG1879), lacking the predicted inner membrane (IM)-associated patatin/PLA2 superfamily member PG1879, did not exhibit a death phase, but instead a prolonged stationary phase. The surviving cells exhibited intact cell membranes and 8-day-old culture regrowth. Contrastingly, the wild type entered death phase, showed a compromised IM and did not regrow under identical conditions. Lipidomic analysis revealed 29 lipid classes, with 16 being novel, and common membrane lipid remodelling that enabled survival during stationary phase. The remodelling involved upregulation of dihydroceramide-containing sphingolipids, in addition to serineglycine dipeptide-containing acyl-oxyacyl lipids (SGL). A PG1879-dependent mass production of Lyso SGL 17:0_OH initiated the death phase by O-deacylation of its acylated counterpart SGL 17:0_OH [15:0].