TABLE 1

Inducing cues of the Rcs and Cpx envelope stress response systems

System induced by stressCue typeCues
CpxNlpE dependentnlpE overexpression (32); artificial mislocalization of NlpE (37, 39); adhesion of stationary phase cells to hydrophobic glass (49, 50); adhesion of stationary phase EHEC cells to undifferentiated epithelial cells (50)
NlpE independentOverproduction of PapE and PapG pilus subunits in the absence of cognate chaperone (59); alkaline pH (Cpx activation shown in reference 60 and NlpE independence from unshown data in reference 59); stationary phase growth (Cpx activation shown in references 59 and 61 and NlpE independence from unshown data in reference 59); lipid II accumulation (Cpx activation shown in reference 62 and NlpE independence from unshown data in reference 59); lack of phosphatidylglycerol or phosphatidylethanolamine (63, 64); EDTA (Cpx activation shown in reference 65 and NlpE independence from unshown data in reference 59); drugs targeting PG synthesis (mecillinam, cephalexin, and A22 [37])
Undetermined role of NlpELoss of 4 PBPs (involved in PG synthesis) (66); overproduction of type IV pilus subunit (67); CuSO4 (68); ΔdegP (69); high osmolarity (65, 70, 71); Curli overproduction and ompR mutation (71); IM stress due to lack of YidC, lack of protease FtsH or HtpX, or accumulation of IM substrates of FtsH like SecY or SecY mutations (72, 73); indole, ethanol, and dibucaine (65); mammalian PG recognition proteins and gentamicin (74); ΔcpxP (59)
RcsRcsF dependentrcsF overexpression (24); artificial mislocalization of RcsF (29); mutation in the LPS biosynthesis pathway (deep rough rfa mutants) (26); cationic antimicrobial peptides, including polymyxin B (29, 46); treatments targeting the PG (lysozyme [47], the β-lactams mecillinam and cefsulodin [48], and MreB inhibitor A22 [16]); defective lipoprotein sorting due to lack of the periplasmic chaperone LolA or dominant-negative LolA mutant (36) or to inhibition of lipoprotein signal peptidase LspA by globomycin 38; lack of the periplasmic chaperone SurA involved in OM biogenesis (30); low levels of BamA in a bamA101 strain (16); mutation (pgsA) in phospholipid biosynthesis leading to lack of phosphatidylglycerol and cardiolipin (28); lack of membrane-derived oligosaccharides (mdo mutations) (data not shown in reference 30); a set of multicopy inducers (from reference 25) (26); growth in excess zinc at high temperature (27)
RcsF independentOverproduction of the IM protein DjlA (28), which acts as an Rcs inhibitor under native expression levels (75); overproduction of the putative lipoprotein YpdI (76)
Undetermined role of RcsFLoss of 4 PBPs (involved in PG synthesis) (66); growth on a solid surface (77)