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Zinc uptake system ZnuACB is essential for maintaining pathogenic phenotype of F4ac(+) enterotoxigenic E. coli (ETEC) under a zinc restricted environment

Zinc is the second trace element of living organisms after iron. Given its crucial importance, mammalian hosts restrict the bioavailability of Zinc ions (Zn(2+)) to bacterial pathogens. As a countermeasure, pathogens utilize high affinity Zn(2+) transporters, such as ZnuACB to compete with the host...

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Autores principales: Quan, Guomei, Xia, Pengpeng, Lian, Siqi, Wu, Yunping, Zhu, Guoqiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7539401/
https://www.ncbi.nlm.nih.gov/pubmed/33028391
http://dx.doi.org/10.1186/s13567-020-00854-1
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author Quan, Guomei
Xia, Pengpeng
Lian, Siqi
Wu, Yunping
Zhu, Guoqiang
author_facet Quan, Guomei
Xia, Pengpeng
Lian, Siqi
Wu, Yunping
Zhu, Guoqiang
author_sort Quan, Guomei
collection PubMed
description Zinc is the second trace element of living organisms after iron. Given its crucial importance, mammalian hosts restrict the bioavailability of Zinc ions (Zn(2+)) to bacterial pathogens. As a countermeasure, pathogens utilize high affinity Zn(2+) transporters, such as ZnuACB to compete with the host for zinc. It is essential for bacteria to maintain zinc homeostasis and thus maintain their physiology and pathogenesis. In an attempt to uncover the zinc transporter in F4(+) enterotoxigenic E. coli (ETEC) C83902, we analyzed two RNA-seq data sets of bacteria samples when different zinc treatments (restriction or abundance) were applied. Considering data revealing that the high affinity zinc uptake system ZnuACB acts as the main transporter in ETEC C83902 to resist zinc deficiency, we deleted znuACB genes to study the role of them in ETEC C83902. The deletion of znuACB genes results in growth perturbation and a sharp decrease in the ability of biofilm formation and adhesion of bacteria in vitro. Taking the data together, this study demonstrates that the ZnuACB system is required for ETEC C83902 to acquire zinc, which highly contributes to ETEC pathogenicity as well.
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spelling pubmed-75394012020-10-08 Zinc uptake system ZnuACB is essential for maintaining pathogenic phenotype of F4ac(+) enterotoxigenic E. coli (ETEC) under a zinc restricted environment Quan, Guomei Xia, Pengpeng Lian, Siqi Wu, Yunping Zhu, Guoqiang Vet Res Research Article Zinc is the second trace element of living organisms after iron. Given its crucial importance, mammalian hosts restrict the bioavailability of Zinc ions (Zn(2+)) to bacterial pathogens. As a countermeasure, pathogens utilize high affinity Zn(2+) transporters, such as ZnuACB to compete with the host for zinc. It is essential for bacteria to maintain zinc homeostasis and thus maintain their physiology and pathogenesis. In an attempt to uncover the zinc transporter in F4(+) enterotoxigenic E. coli (ETEC) C83902, we analyzed two RNA-seq data sets of bacteria samples when different zinc treatments (restriction or abundance) were applied. Considering data revealing that the high affinity zinc uptake system ZnuACB acts as the main transporter in ETEC C83902 to resist zinc deficiency, we deleted znuACB genes to study the role of them in ETEC C83902. The deletion of znuACB genes results in growth perturbation and a sharp decrease in the ability of biofilm formation and adhesion of bacteria in vitro. Taking the data together, this study demonstrates that the ZnuACB system is required for ETEC C83902 to acquire zinc, which highly contributes to ETEC pathogenicity as well. BioMed Central 2020-10-07 2020 /pmc/articles/PMC7539401/ /pubmed/33028391 http://dx.doi.org/10.1186/s13567-020-00854-1 Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research Article
Quan, Guomei
Xia, Pengpeng
Lian, Siqi
Wu, Yunping
Zhu, Guoqiang
Zinc uptake system ZnuACB is essential for maintaining pathogenic phenotype of F4ac(+) enterotoxigenic E. coli (ETEC) under a zinc restricted environment
title Zinc uptake system ZnuACB is essential for maintaining pathogenic phenotype of F4ac(+) enterotoxigenic E. coli (ETEC) under a zinc restricted environment
title_full Zinc uptake system ZnuACB is essential for maintaining pathogenic phenotype of F4ac(+) enterotoxigenic E. coli (ETEC) under a zinc restricted environment
title_fullStr Zinc uptake system ZnuACB is essential for maintaining pathogenic phenotype of F4ac(+) enterotoxigenic E. coli (ETEC) under a zinc restricted environment
title_full_unstemmed Zinc uptake system ZnuACB is essential for maintaining pathogenic phenotype of F4ac(+) enterotoxigenic E. coli (ETEC) under a zinc restricted environment
title_short Zinc uptake system ZnuACB is essential for maintaining pathogenic phenotype of F4ac(+) enterotoxigenic E. coli (ETEC) under a zinc restricted environment
title_sort zinc uptake system znuacb is essential for maintaining pathogenic phenotype of f4ac(+) enterotoxigenic e. coli (etec) under a zinc restricted environment
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7539401/
https://www.ncbi.nlm.nih.gov/pubmed/33028391
http://dx.doi.org/10.1186/s13567-020-00854-1
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