Activates the transcription of the eut operon, allowing utilization of ethanolamine (EA). Positively regulates its own transcription (Probable) (PubMed:1328159, PubMed:8113167). Probably binds EA and vitamin B12 as effectors (Probable). Competes with ethanolamine ammonia-lysase (EAL, the first enzyme in the EA degradation pathway) for adenosylcobalamin (PubMed:8113167). Ethanolamine-associated signaling mediated via this protein, but not EA degradation, impacts S.typhimurium survival within macrophages. Binds the promoter of ssrB and eutS in vitro; in mouse infection models binding to ssrB probably induces all 4 operons of pathogenicity island SPI-2 (PubMed:26565973). Expression of the eut operon allows this bacteria to use ethanolamine (EA) as a carbon, nitrogen and energy source. It relies on cobalamin (vitamin B12) both as a cofactor for the ethanolamine ammonia-lyase (EAL) activity and to induce the operon (PubMed:3045078). EA enhances bacterial survival in macrophages in a concentration-dependent manner, suggesting it is an important nutrient in infection (PubMed:29531136). Amine and polyamine degradation; ethanolamine degradation. Part of the 17-gene eut operon transcribed from a single promoter, positively regulates its own expression, induced by ethanolamine and adenosylcobalamin (AdoCbl, vitamin B12). This is the last gene in the operon and has a second weaker promoter that is constitutively transcribed at a low level (PubMed:10464203, PubMed:3045078, PubMed:1328159, PubMed:26565973) (Probable). Subject to catabolite repression; expression is substantially lower during growth on glucose than during growth versus succinate. Catabolite repression is overcome by adding exogenous cAMP to the glucose growth media (PubMed:1328159). Induced after phagocytosis by mouse RAW macrophages and in spleen in mouse infection; the whole eut operon is not induced (PubMed:26565973). Mutations prevent expression of the entire eut operon (PubMed:2656649). No phenotype during bacterial growth in vitro. About 10-fold outcompeted by wild-type in mouse intestines at 2 and 4 days following oral infection. Loss of induction of pathogenicity island SPI-2 in mouse macrophages (PubMed:26684793). About 25% reduction in survival in mouse macrophage assays. Bacteria growth is not enhanced by exogenous EA in macrophage survival assays (PubMed:29531136).