The molecular mechanism for carbon catabolite repression of the chitin response in Vibrio cholerae.


Journal

PLoS genetics
ISSN: 1553-7404
Titre abrégé: PLoS Genet
Pays: United States
ID NLM: 101239074

Informations de publication

Date de publication:
05 2023
Historique:
received: 29 09 2022
accepted: 30 04 2023
revised: 24 05 2023
medline: 26 5 2023
pubmed: 12 5 2023
entrez: 12 5 2023
Statut: epublish

Résumé

Vibrio cholerae is a facultative pathogen that primarily occupies marine environments. In this niche, V. cholerae commonly interacts with the chitinous shells of crustacean zooplankton. As a chitinolytic microbe, V. cholerae degrades insoluble chitin into soluble oligosaccharides. Chitin oligosaccharides serve as both a nutrient source and an environmental cue that induces a strong transcriptional response in V. cholerae. Namely, these oligosaccharides induce the chitin sensor, ChiS, to activate the genes required for chitin utilization and horizontal gene transfer by natural transformation. Thus, interactions with chitin impact the survival of V. cholerae in marine environments. Chitin is a complex carbon source for V. cholerae to degrade and consume, and the presence of more energetically favorable carbon sources can inhibit chitin utilization. This phenomenon, known as carbon catabolite repression (CCR), is mediated by the glucose-specific Enzyme IIA (EIIAGlc) of the phosphoenolpyruvate-dependent phosphotransferase system (PTS). In the presence of glucose, EIIAGlc becomes dephosphorylated, which inhibits ChiS transcriptional activity by an unknown mechanism. Here, we show that dephosphorylated EIIAGlc interacts with ChiS. We also isolate ChiS suppressor mutants that evade EIIAGlc-dependent repression and demonstrate that these alleles no longer interact with EIIAGlc. These findings suggest that EIIAGlc must interact with ChiS to exert its repressive effect. Importantly, the ChiS suppressor mutations we isolated also relieve repression of chitin utilization and natural transformation by EIIAGlc, suggesting that CCR of these behaviors is primarily regulated through ChiS. Together, our results reveal how nutrient conditions impact the fitness of an important human pathogen in its environmental reservoir.

Identifiants

pubmed: 37172034
doi: 10.1371/journal.pgen.1010767
pii: PGENETICS-D-22-01115
pmc: PMC10208484
doi:

Substances chimiques

Chitin 1398-61-4
Oligosaccharides 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

e1010767

Subventions

Organisme : NIGMS NIH HHS
ID : R35 GM128674
Pays : United States
Organisme : NIGMS NIH HHS
ID : R01 GM130874
Pays : United States

Informations de copyright

Copyright: © 2023 Green et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Déclaration de conflit d'intérêts

The authors have declared that no competing interests exist.

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Auteurs

Virginia E Green (VE)

Department of Biology, Indiana University, Bloomington, Indiana, United States of America.

Catherine A Klancher (CA)

Department of Biology, Indiana University, Bloomington, Indiana, United States of America.

Shouji Yamamoto (S)

Department of Bacteriology I, National Institute of Infectious Diseases, Tokyo, Japan.

Ankur B Dalia (AB)

Department of Biology, Indiana University, Bloomington, Indiana, United States of America.

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