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

Nick D. Pokorzynski, Nathan D. Hatch, Scot P. Ouellette and Rey A. Carabeo ()
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Nick D. Pokorzynski: Washington State University
Nathan D. Hatch: University of Nebraska Medical Center
Scot P. Ouellette: University of Nebraska Medical Center
Rey A. Carabeo: University of Nebraska Medical Center

Nature Communications, 2020, vol. 11, issue 1, 1-15

Abstract: Abstract 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 (PtrpR), while the IGR harbors an alternative promoter (PtrpBA) and an operator sequence for the iron-dependent repressor YtgR to regulate trpBA expression. Here, we report that YtgR repression at PtrpBA 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 PtrpBA. 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.

Date: 2020
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DOI: 10.1038/s41467-020-20181-5

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