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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

The Zinc Transporter ZnuABC Is Critical for the Virulence of Chromobacterium violaceum and Contributes to Diverse Zinc-Dependent Physiological Processes

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Santos, Renato E. R. S. [1] ; da Silva Junior, Waldir P. [1] ; Harrison, Simone [2, 3, 4] ; Skaar, Eric P. [5, 6] ; Chazin, Walter J. [2, 3, 4] ; da Silva Neto, Jose F. [1]
Total Authors: 6
[1] Univ Sao Paulo, Fac Med Ribeirao Preto, Dept Biol Celular & Mol & Bioagentes Patogen, Ribeirao Preto, SP - Brazil
[2] Vanderbilt Univ, Dept Biochem, Nashville, TN 37232 - USA
[3] Vanderbilt Univ, Dept Chem, Nashville, TN - USA
[4] Vanderbilt Univ, Med Ctr, Ctr Struct Biol, Nashville, TN - USA
[5] Vanderbilt Univ, Dept Pathol Microbiol & Immunol, Med Ctr, Nashville, TN - USA
[6] Vanderbilt Univ, Vanderbilt Inst Infect Immunol & Inflammat, Med Ctr, Nashville, TN - USA
Total Affiliations: 6
Document type: Journal article
Source: Infection and Immunity; v. 89, n. 11 NOV 2021.
Web of Science Citations: 0

Chromobacterium violaceum is a ubiquitous environmental bacterium that causes sporadic life-threatening infections in humans. How C. violaceum acquires zinc to colonize environmental and host niches is unknown. In this work, we demonstrated that C. violaceum employs the zinc uptake system ZnuABC to overcome zinc limitation in the host, ensuring the zinc supply for several physiological demands. Our data indicated that the C. violaceum ZnuABC transporter is encoded in a zur-CV\_RS15045-CV\_RS15040-znuCBA operon. This operon was repressed by the zinc uptake regulator Zur and derepressed in the presence of the host protein calprotectin (CP) and the synthetic metal chelator EDTA. A. Delta znuCBA mutant strain showed impaired growth under these zinc-chelated conditions. Moreover, the deletion of znuCBA provoked reductions in violacein production, swimming motility, biofilm formation, and bacterial competition. Remarkably, the Delta znuCBA mutant strain was highly attenuated for virulence in an in vivo mouse infection model and showed low capacities to colonize the liver, grow in the presence of CP, and resist neutrophil killing. Overall, our findings demonstrate that ZnuABC is essential for C. violaceum virulence, contributing to subversion of zinc-based host nutritional immunity. (AU)

FAPESP's process: 17/03342-0 - The Fur family of transcription factors and the response to iron and zinc in Chromobacterium violaceum
Grantee:Renato Elias Rodrigues de Souza Santos
Support type: Scholarships in Brazil - Doctorate
FAPESP's process: 20/00259-8 - Role of secretion systems of Chromobacterium violaceum in the interaction with the host and other bacteria
Grantee:José Freire da Silva Neto
Support type: Regular Research Grants
FAPESP's process: 18/01388-6 - Iron homeostasis in Chromobacterium violaceum: regulatory mechanisms, uptake systems and role in virulence
Grantee:José Freire da Silva Neto
Support type: Regular Research Grants
FAPESP's process: 18/14737-9 - Role of the ZnuCBA transporter in zinc homeostasis in Chromobacterium violaceum
Grantee:Waldir Paulo da Silva Júnior
Support type: Scholarships in Brazil - Scientific Initiation