Mutations to essential orphan response regulator HP1043 of Helicobacter pylori result in growth-stage regulatory defects.

ABSTRACT: Helicobacter pylori establishes lifelong infections of the gastric mucosa, a niche considered hostile to most microbes. While responses to gastric acidity and local inflammation are understood, little is known as to how they are integrated into homeostatic control of cell division and growth-stage gene expression. Here we investigate the essential orphan response regulator HP1043, a member of the OmpR/PhoB subfamily of transcriptional regulators that is unique to the Epsilonproteobacteria and that lacks phosphorylation domains. To test the hypothesis that conformational changes in the homodimer might lead to defects in gene expression, we sought mutations that might alter DNA-binding efficiency. Two introduced mutations (C215S, C221S) C terminal to the DNA-binding domain of HP1043 (HP1043C

SUBMITTER: Olekhnovich IN 

PROVIDER: S-EPMC3647984 | biostudies-literature | 2013 May

REPOSITORIES: biostudies-literature