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

Author:

Pokorzynski Nick D.ORCID,Hatch Nathan D.,Ouellette Scot P.ORCID,Carabeo Rey A.ORCID

Abstract

AbstractThetrpoperon 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.

Funder

U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases

U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences

Achievement Rewards for College Scientists Foundation

National Science Foundation

Publisher

Springer Science and Business Media LLC

Subject

General Physics and Astronomy,General Biochemistry, Genetics and Molecular Biology,General Chemistry

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