FIG. 1.
MucA-AlgU is the central regulatory pathway controlling the expression of the mucoid phenotype in P. aeruginosa. In mucA mutants, AlgU is not repressed (32) and activates transcription of downstream promoters. The algU gene is transcribed by five promoters, two of which (P1 and P3) are dependent on AlgU (46). AlgU activates transcription of algB, algR, and amrZ, whose gene products participate in transcriptional activation of PalgD (4, 38, 56). In a muc-23 mucoid mutant, RpoN has also been shown to bind to PalgD and activate or repress transcription under certain environmental conditions (7). AlgU also activates transcription of PalgD (57). Activation of transcription at PalgD results in alginate overproduction and a mucoid phenotype. MucA is the anti-σ-factor that sequesters AlgU(T) (46). The predicted protease AlgW can cleave MucA, which results in derepression of AlgU. Overexpression of the periplasmic peptide MucE results in mucoidy due to activation of AlgW (43), which leads to degradation of MucA. Cell wall inhibitors such as d-cycloserine have been shown to upregulate AlgW-dependent transcription at PalgD (54).