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Chlamydia trachomatis  is an obligate intracellular human pathogen that exhibits stage-specific gene transcription throughout a biphasic developmental cycle. The mechanisms that control modulation in transcription and associated phenotypic changes are poorly understood. This study provides evidence that a switch-protein kinase regulatory network controls availability of σ 66   ,  the main sigma subunit for transcription in  Chlamydia .  In vitro  analysis revealed that a putative switch-protein kinase regulator, RsbW, is capable of interacting directly with σ 66 , as well as phosphorylating its own antagonist, RsbV1, rendering it inactive. Conversely, the putative PP2C-like phosphatase domain of chlamydial RsbU was capable of reverting RsbV1 into its active state. Recent advances in genetic manipulation of  Chlamydia  were employed to inactivate  rsbV1 , as well as to increase the expression levels of  rsbW  or  rsbV1 ,  in vivo . Representative σ 66 -dependent gene transcription was repressed in the absence of  rsbV1  or upon increased expression of RsbW, and increased upon elevated expression of RsbV1. These effects on housekeeping transcription were also correlated to several measures of growth and development. A model is proposed where the relative levels of active antagonist (RsbV1) and switch-protein anti-sigma factor (RsbW) control the availability of σ 66  and subsequently act as a molecular 'throttle' for  Chlamydia  growth and development.

plos pathogens

The Rsb Phosphoregulatory Network Controls Availability of the Primary Sigma Factor in Chlamydia trachomatis and Influences the Kinetics of Growth and Development