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The obligate intracellular human pathogen  Chlamydia trachomatis  undergoes a complex developmental program involving transition between two forms: the infectious elementary body (EB), and the rapidly dividing reticulate body (RB). However, the regulators controlling this development have not been identified. To uncover potential regulators of transcription in  C. trachomatis , we screened a  C. trachomatis  genomic library for sequences encoding proteins that interact with RNA polymerase (RNAP). We report the identification of one such protein, CT663, which interacts with the β and σ subunits of RNAP. Specifically, we show that CT663 interacts with the flap domain of the β subunit (β-flap) and conserved region 4 of the primary σ subunit (σ 66  in  C. trachomatis ). We find that CT663 inhibits σ 66 -dependent (but not σ 28 -dependent) transcription in vitro, and we present evidence that CT663 exerts this effect as a component of the RNAP holoenzyme. The analysis of  C. trachomatis -infected cells reveals that CT663 begins to accumulate at the commencement of the RB-to-EB transition. Our findings suggest that CT663 functions as a negative regulator of σ 66 -dependent transcription, facilitating a global change in gene expression. The strategy used here is generally applicable in cases where genetic tools are unavailable.

genes and development

A regulator from <i>Chlamydia trachomatis</i> modulates the activity of RNA polymerase through direct interaction with the β subunit and the primary σ subunit

A regulator from Chlamydia trachomatis modulates the activity of RNA polymerase through direct interaction with the β subunit and the primary σ subunit