Figure 5.

Overview of the lactococcal cell envelope stress response. Upon cell wall damage (A), the CesSR two component system (pink shapes) is activated. The response regulator CesR is phosphorylated by the histidine kinase CesS (black arrows) and triggers induction of the yjbBcesSR operon, llmg2164_2163 operon and spxB, among other genes. SpxB (green sphere) binds to RNAP and drives transcription of oatA. TmrA, Llmg_1703 and Llmg_0514 (yellow, blue and purple spheres, respectively) are SpxB paralogs which may fine tune SpxB binding to RNAP and transcription of other genes (X). Resistance to cell wall damage (B) is attained by SpxB-induced overproduction of O-acetyl-transferase OatA that acetylates peptidoglycan (i.e. protection from hydrolysis). Changes in the overall architecture of the cell wall, presumably produced by displacement of CWPSs from their attachment sites, may also contribute to resistance. The membrane proteins YjbB (grey) and Llmg2163 (golden yellow) could modulate the activity of CesS (dotted arrows) but their function remains to be elucidated (see text for further details). PG, peptidoglycan; CM, cytoplasmic membrane; H, PG hydrolase (lysozyme); α RNAP, RNA polymerase and α subunit; CWPS, cell wall polysaccharide; PSP, polysaccharide pellicle; black dots (•), sites of PG O-acetylation. Adapted from Veiga et al. 2007, published in the Journal of Biological Chemistry. © the American Society for Biochemistry and Molecular Biology.