Anaerobic adaptation in Pseudomonas aeruginosa: definition of the Anr and Dnr regulons

Abstract

SummaryThe anaerobic metabolism of the opportunistic pathogen Pseudomonas aeruginosa is important for growth and biofilm formation during persistent infections. The two Fnr-type transcription factors Anr and Dnr regulate different parts of the underlying network in response to oxygen tension and NO. Little is known about all members of the Anr and Dnr regulons and the mediated immediate response to oxygen depletion. Comprehensive transcriptome and bioinformatics analyses in combination with a limited proteome analyses were used for the investigation of the P. aeruginosa response to an immediate oxygen depletion and for definition of the corresponding Anr and Dnr regulons. We observed at first the activation of fermentative pathways for immediate energy generation followed by induction of alternative respiratory chains. A solid position weight matrix model was deduced from the experimentally identified Anr boxes and used for identification of 170 putative Anr boxes in potential P. aeruginosa promoter regions. The combination with the experimental data unambiguously identified 130 new members for the Anr and Dnr regulons. The basis for the understanding of two regulons of P. aeruginosa central to biofilm formation and infection is now defined.

Low oxygen induces the type III secretion system in Pseudomonas aeruginosa via modulation of the small RNAs rsmZ and rsmY

“…However, the important question of whether oxygen availability influences the T3SS in P. aeruginosa remains to be addressed. While transcriptome analyses of the molecular response of P. aeruginosa to low oxygen have not yet identified any alteration in T3SS-associated gene expression (AlvarezOrtega & Harwood, 2007;Trunk et al, 2010), T3SS-associated gene expression is induced in anaerobic biofilms (Waite & Curtis, 2009). …”

“…Thus, CF-associated pathogens may only survive and persist in the infected lung by adapting to limiting oxygen stress. P. aeruginosa perceives and responds to low oxygen stress via the global anaerobic stress response regulator Anr (Sawers, 1991;Trunk et al, 2010;Zimmermann et al, 1991). Anr is a homologue of the Escherichia coli anaerobic response master regulator FNR, and it functions by regulating a large number of genes required for anaerobic respiration, including dnr and the narXL two-component system (Sawers, 1991;Trunk et al, 2010;Zimmermann et al, 1991).…”

“…P. aeruginosa perceives and responds to low oxygen stress via the global anaerobic stress response regulator Anr (Sawers, 1991;Trunk et al, 2010;Zimmermann et al, 1991). Anr is a homologue of the Escherichia coli anaerobic response master regulator FNR, and it functions by regulating a large number of genes required for anaerobic respiration, including dnr and the narXL two-component system (Sawers, 1991;Trunk et al, 2010;Zimmermann et al, 1991). During lowoxygen stress, the NarL response regulator is involved in coordinating energy metabolism through induction of nitrate metabolism (Palmer et al, 2007;Schreiber et al, 2007;Sharma et al, 2006) and repression of less efficient modes of energy generation such as pyruvate and arginine fermentation (Benkert et al, 2008).…”

Global regulator Anr represses PlcH phospholipase activity in Pseudomonas aeruginosa when oxygen is limiting

“…A sequence identical to that recognized by the oxygensensitive transcriptional regulator Anr is present within the plcH promoter region (Galimand et al, 1991;Trunk et al, 2010). Anr mainly acts as a regulator of gene expression under micro-oxic and anoxic conditions (Arai et al, 1995;Kawakami et al, 2010;Lu et al, 1999;Ye et al, 1995), and its activity increases as oxygen tensions decrease.…”

“…The histone-like nucleoid-associated proteins MvaT and MvaU were both shown to bind and inhibit the transcription of the plcH ORF in P. aeruginosa (Castang et al, 2008). Several publications have reported that a canonical Anr consensus sequence is positioned within the plcH promoter (Galimand et al, 1991;Trunk et al, 2010), suggesting a role for negative regulation of plcH by Anr. However, this regulatory scheme has not been established.…”