The HspR repressor regulates transcription of the groESL, hrcA-grpE-dnaK, and cbpA-hspR-orf operons of Helicobacter pylori. Here we show that two of the HspR-regulated operons, namely, the groESL and dnaK operons, encoding the major cellular chaperone machineries are also regulated by the H. pylori homologue of the HrcA repressor. Similarly to the hspR mutation, deletion of the hrcA gene also leads to complete derepression of the Pgro and Phrc promoters. The presence of both HspR and HrcA is therefore necessary for regulated transcription from these promoters. HrcA binds directly to Pgro and Phrc, likely contacting two inverted repeats with similarity to the CIRCE motif, which are present on both promoters. HrcA regulation is, however, shown to depend on binding of the HspR protein, since deletion of the HspR-binding site of the Pgro promoter leads to loss of heat inducibility of this promoter. In contrast, transcription from the Pcbp promoter is regulated solely by HspR. HspR is also shown to form oligomers in vivo through a stretch of hydrophobic repeats between amino acid positions 66 and 97. The implications of these findings for the elucidation of the networks regulating heat shock gene expression in H. pylori are discussed.

Dual Control of Helicobacter pylori Heat Shock Gene Transcription by HspR and HrcA.

DANIELLI, ALBERTO;RONCARATI, DAVIDE;SCARLATO, VINCENZO
2004

Abstract

The HspR repressor regulates transcription of the groESL, hrcA-grpE-dnaK, and cbpA-hspR-orf operons of Helicobacter pylori. Here we show that two of the HspR-regulated operons, namely, the groESL and dnaK operons, encoding the major cellular chaperone machineries are also regulated by the H. pylori homologue of the HrcA repressor. Similarly to the hspR mutation, deletion of the hrcA gene also leads to complete derepression of the Pgro and Phrc promoters. The presence of both HspR and HrcA is therefore necessary for regulated transcription from these promoters. HrcA binds directly to Pgro and Phrc, likely contacting two inverted repeats with similarity to the CIRCE motif, which are present on both promoters. HrcA regulation is, however, shown to depend on binding of the HspR protein, since deletion of the HspR-binding site of the Pgro promoter leads to loss of heat inducibility of this promoter. In contrast, transcription from the Pcbp promoter is regulated solely by HspR. HspR is also shown to form oligomers in vivo through a stretch of hydrophobic repeats between amino acid positions 66 and 97. The implications of these findings for the elucidation of the networks regulating heat shock gene expression in H. pylori are discussed.
G. SPOHN; A. DANIELLI; D. RONCARATI; I. DELANY; R. RAPPUOLI; V. SCARLATO
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11585/2472
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