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Title: The iron-dependent repressor YtgR is a tryptophan-dependent attenuator of the trpRBA operon in Chlamydia trachomatis

Thetrpoperon ofChlamydia trachomatisis organized differently from other model bacteria. It containstrpR, an intergenic region (IGR), and the biosynthetictrpBandtrpAopen-reading frames. TrpR is a tryptophan-dependent repressor that regulates the major promoter (PtrpR), while the IGR harbors an alternative promoter (PtrpBA) and an operator sequence for the iron-dependent repressor YtgR to regulatetrpBAexpression. Here, we report that YtgR repression at PtrpBAis also dependent on tryptophan by regulating YtgR levels through a rare triple-tryptophan motif (WWW) in the YtgCR precursor. Inhibiting translation during tryptophan limitation at the WWW motif subsequently promotes Rho-independent transcription termination ofytgR, thereby de-repressing PtrpBA. Thus, YtgR represents an alternative strategy to attenuatetrpBAexpression, expanding the repertoire fortrpoperon attenuation beyond TrpL- and TRAP-mediated mechanisms described in other bacteria. Furthermore, repurposing the iron-dependent repressor YtgR underscores the fundamental importance of maintaining tryptophan-dependent attenuation of thetrpRBAoperon.

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Nature Communications
Nature Publishing Group
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National Science Foundation
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