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The  trp  operon of  Chlamydia trachomatis  is organized differently from other model bacteria. It contains  trpR , an intergenic region (IGR), and the biosynthetic  trpB  and  trpA  open-reading frames. TrpR is a tryptophan-dependent repressor that regulates the major promoter (P  trpR  ), while the IGR harbors an alternative promoter (P  trpBA  ) and an operator sequence for the iron-dependent repressor YtgR to regulate  trpBA  expression. Here, we report that YtgR repression at P  trpBA   is 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 of  ytgR , thereby de-repressing P  trpBA  . Thus, YtgR represents an alternative strategy to attenuate  trpBA  expression, expanding the repertoire for  trp  operon 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 the  trpRBA  operon.

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