Abstract
During infection, pathogens are starved of essential nutrients such as iron and tryptophan by host immune effectors. Without conserved global stress response regulators, how the obligate intracellular bacterium Chlamydia trachomatis arrives at a physiologically similar 'persistent' state in response to starvation of either nutrient remains unclear. Here, we report on the iron-dependent regulation of the trpRBA tryptophan salvage pathway in C. trachomatis. Iron starvation specifically induces trpBA expression from a novel promoter element within an intergenic region flanked by trpR and trpB. YtgR, the only known iron-dependent regulator in Chlamydia, can bind to the trpRBA intergenic region upstream of the alternative trpBA promoter to repress transcription. Simultaneously, YtgR binding promotes the termination of transcripts from the primary promoter upstream of trpR. This is the first description of an iron-dependent mechanism regulating prokaryotic tryptophan biosynthesis that may indicate the existence of novel approaches to gene regulation and stress response in Chlamydia.
Highlights
IntroductionMany pathogenic bacteria must siphon nutrients from their hosts, such as nucleotides, amino acids and biometals (Brown et al, 2008; Eisenreich et al, 2010; Ray et al, 2009; Skaar, 2010)
Nutrient acquisition is critical for the success of pathogenic bacteria
We provide a mechanistic explanation for the specific iron-limited induction of trpBA expression mediated by the repressor YtgR, representing a novel instance of integrated stress adaptation in Chlamydia
Summary
Many pathogenic bacteria must siphon nutrients from their hosts, such as nucleotides, amino acids and biometals (Brown et al, 2008; Eisenreich et al, 2010; Ray et al, 2009; Skaar, 2010). Bacterial pathogens have evolved sophisticated molecular mechanisms to respond to nutrient deprivation, involving increasingly complex and sophisticated nutrient-sensing regulatory networks. These stress response mechanisms are essential for pathogens to avoid clearance by the immune system. Stress responses in the obligate intracellular bacterium Chlamydia trachomatis are relatively poorly characterized, leaving unanswered many fundamental questions about the biology of this pathogen
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