Proteomic mapping of a suppressor of non‐chemotactic cheW mutants reveals that Helicobacter pylori contains a new chemotaxis protein

Terry, Karianne; Go, Alvin C; Ottemann, Karen M.

doi:10.1111/j.1365-2958.2006.05283.x

Cited by 37 publications

(46 citation statements)

References 32 publications

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“…CheB protein lacks a CheY-like receiver domain, while CheA protein contains an additional C-terminal domain homologous to CheY. C. jejuni also encodes a CheV protein, similar to CheV in B. subtilis (Fredrick and Helmann 1994) and a putative analog of CheZ like Helicobacter pylori (Terry et al 2006). …”

Section: Introductionmentioning

confidence: 98%

Comparative in silico analysis of chemotaxis system of Campylobacter fetus

2011

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Chemoreceptor and chemotaxis signal transduction cascade genes of C. fetus subsp. fetus 82-40 show high level of similarity to that in C. jejuni and appears to include sixteen diverse transducer-like protein (tlp) genes that appear similar to nine of the twelve tlp genes in the C. jejuni NCTC 11168 with a percent identity ranging from 15 to 50%. Sixteen putative C. fetus 82-40 tlp genes belong to three classes: A, B, and C, as well as an aerotaxis gene, based on their predicted structure. C. fetus subsp. fetus 82-40 chemoreceptor and chemotaxis signal transduction pathway genes have close phylogenetic relationship of chemotaxis genes between Campylobacteraceae and Helicobacteraceae.

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Section: Introductionmentioning

confidence: 98%

Comparative in silico analysis of chemotaxis system of Campylobacter fetus

2011

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“…In Escherichia coli, the CheY-P phosphatase CheZ is absolutely necessary for chemotaxis (16). However, CheZ has only been found in proteobacterial genomes (17,18). The CheC, FliY, and CheX protein family members have been shown to be CheY-P phosphatases and are found throughout the Bacteria and Archaea domains (19 -21).…”

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confidence: 99%

The CheC Phosphatase Regulates Chemotactic Adaptation through CheD

Muff¹,

Ordal

2007

Journal of Biological Chemistry

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The bacterial chemotaxis system is one of the most extensively studied signal transduction systems in biology. The response regulator CheY controls flagellar rotation and is phosphorylated by the CheA histidine kinase to its active form. CheC is a CheY-P phosphatase, and this activity is enhanced in a CheC-CheD heterodimer. CheC is also critical for chemotactic adaptation, the return to the prestimulus system state despite persistent attractant concentrations. Here, CheC point mutants were examined in Bacillus subtilis for in vivo complementation and in vitro activity. The mutants were identified separating the three known abilities of CheC: CheD binding, CheY-P binding, and CheY-P phosphatase activity. Remarkably, the phosphatase ability was not as critical to the in vivo function of CheC as the ability to bind both CheY-P and CheD. Additionally, it was confirmed that CheY-P increases the affinity of CheC for CheD, the later of which is known to be necessary for receptor activation of CheA. These data suggest a model of CheC as a CheY-P-induced regulator of CheD. Here, CheY-P would cause CheC to sequester CheD from the chemoreceptors, inducing adaptation of the chemotaxis system. This model represents the first plausible means for feedback from the output of the system, CheY-P, to the receptors.

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“…Originally, the NCTC11168 genome was thought not to contain a CheZ protein which stimulates dephosphorylation of CheY [20]. However, a recent study in H. pylori identified a putative CheZ protein (HP0170) which also has an ortholog (Cj0700) in C. jejuni [21]. The C. jejuni genome also encodes nine so-called onecomponent regulators, proteins containing a DNA-binding domain linked directly to signal-sensing domain.…”

Section: Gene Regulationmentioning

confidence: 98%

Genomics of Thermophilic Campylobacter Species

Gaskin¹,

Reuter²,

Shearer³

et al. 2009

Microbial Pathogenomics

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The thermophilic Campylobacter species C. jejuni and C. coli are important human pathogens, which are major causes of bacterial gastroenteritis. The recent progress in genomics techniques has allowed for a rapid increase in our knowledge of the molecular biology of Campylobacter species, but needs to be matched by concurrent increases in our understanding of the unique biology of these organisms. Campylobacter species display significant levels of genomic variation via natural transformation, phase variation, plasmid transfer and infection with bacteriophages, and this poses a continuous challenge for studies on pathogenesis, physiology, epidemiology and evolution of Campylobacter. In this chapter we will review the current state of the art of the genomics of thermophilic Campylobacter species, and opportunities where genomics can further contribute to our understanding of the biology of these successful human pathogens.

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Proteomic mapping of a suppressor of non‐chemotactic cheW mutants reveals that Helicobacter pylori contains a new chemotaxis protein

Cited by 37 publications

References 32 publications

Comparative in silico analysis of chemotaxis system of Campylobacter fetus

Comparative in silico analysis of chemotaxis system of Campylobacter fetus

The CheC Phosphatase Regulates Chemotactic Adaptation through CheD

Genomics of Thermophilic <i>Campylobacter</i> Species

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