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Coordinating Persistent Infection

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Science  26 Nov 2004:
Vol. 306, Issue 5701, pp. 1441
DOI: 10.1126/science.306.5701.1441c

In patients with cystic fibrosis, chronic infection with the pathogen Pseudomonas aeruginosa is the primary cause of death. During the course of long-lasting infections, bacteria respond to their environment, first expressing a set of genes for infection and initial colonization and later expressing components that favor the formation of biofilms that allow aggregation and protection from host defenses. Goodman et al. screened for two-component system proteins (histidine kinase sensors or phosphate receiver response regulators) that might participate in control of the early or late gene expression programs. They isolated a gene named retS (for regulator of exopolysaccharide and type III secretion). Transcriptional profiling showed that expression of retS enhanced expression of genes encoding virulence factors and decreased expression of genes that enhance synthesis of exopolysaccharides: cell surface components that support the formation of biofilms. The RetS protein has an unusual structure: It contains two dissimilar response regulator receiver domains and lacks a histidine phosphotransfer domain. The authors propose that one or both of the receiver domains may respond to phosphorylation by proteins other than RetS itself, thus allowing RetS to coordinate multiple inputs in the phenotypic response. — LBR

Dev. Cell 7, 745 (2004).

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