Transcriptional regulation of the Pseudomonas aeruginosa type III secretion system

197Citations
Citations of this article
212Readers
Mendeley users who have this article in their library.

This article is free to access.

Abstract

Type III secretion systems (T3SS) function by translocating effector proteins into eukaryotic host cells and are important for the virulence of many Gram-negative bacterial pathogens. Although the secretion and translocation machineries are highly conserved between different species, each pathogen translocates a unique set of effectors that subvert normal host cell physiology to promote pathogenesis. The uniqueness of each pathogen is further reflected in the diversity of mechanisms used to regulate T3SS gene expression. Pseudomonas aeruginosa utilizes a complex set of signalling pathways to modulate T3SS expression in response to extracellular and intracellular cues. Whereas some pathways are dedicated solely to regulating the T3SS, others co-ordinately regulate expression of the T3SS with multiple virulence functions on a global scale. Emerging regulatory themes include coupling of T3SS transcription with type III secretory activity, global regulatory control through modulation of cAMP biosynthesis, repression by a variety of stresses, involvement of multiple two component regulatory systems, and an inverse relationship between T3SS expression and multicellular behaviour. Factors controlling activation of T3SS expression likely contribute to the environmental survival of the organism and to the pathogenesis of acute P. aeruginosa infections. Conversely, active repression of the T3SS might contribute to the persistence of chronic infections. © 2006 The Authors.

Cite

CITATION STYLE

APA

Yahr, T. L., & Wolfgang, M. C. (2006, November). Transcriptional regulation of the Pseudomonas aeruginosa type III secretion system. Molecular Microbiology. https://doi.org/10.1111/j.1365-2958.2006.05412.x

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free