Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form

Chlaraydial GroEL autoregulates its own expression through direct interactions with the HrcA repressor protein

Academic Article
uri icon
  • Overview
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Wilson, A. C.
  • Wu, Chunlei
  • Yates III, John
  • Tan, M.

publication date

  • November 2005

journal

  • Journal of Bacteriology  Journal

abstract

  • In the pathogenic bacterium Chlamydia trachomatis, a transcriptional repressor, HrcA, regulates the major heat shock operons, dnaK and groE. Cellular stress causes a transient increase in transcription of these heat shock operons through relief of HrcA-mediated repression, but the pathway leading to derepression is unclear. Elevated temperature alone is not sufficient, and it is hypothesized that additional chlamydial factors play a role. We used DNA affinity chromatography to purify proteins that interact with HrcA in vivo and identified a higher-order complex consisting of HrcA, GroEL, and GroES. This endogenous HrcA complex migrated differently than recombinant HrcA, but the complex could be disrupted, releasing native HrcA that resembled recombinant HrcA. In in vitro assays, GroEL increased the ability of HrcA to bind to the CIRCE operator and to repress transcription. Other chlamydial heat shock proteins, including the two additional GroEL paralogs present in all chlamydial species, did not modulate HrcA activity.

subject areas

  • Bacterial Proteins
  • Chaperonin 10
  • Chaperonin 60
  • Chlamydia trachomatis
  • Chromatography, Affinity
  • DNA-Binding Proteins
  • Electrophoretic Mobility Shift Assay
  • Gene Expression Regulation, Bacterial
  • Mass Spectrometry
  • Operator Regions, Genetic
  • Protein Binding
  • Repressor Proteins
  • Transcription, Genetic
scroll to property group menus

Identity

PubMed Central ID

  • PMC1272993

International Standard Serial Number (ISSN)

  • 0021-9193

Digital Object Identifier (DOI)

  • 10.1128/jb.187.21.7535-7542.2005

PubMed ID

  • 16237037
scroll to property group menus

Additional Document Info

start page

  • 7535

end page

  • 7542

volume

  • 187

issue

  • 21

©2021 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support