The Contribution of ArsB to Arsenic Resistance in Campylobacter jejuni

dc.contributor.author Shen, Zhangqi
dc.contributor.author Han, Jing
dc.contributor.author Zhang, Qijing
dc.contributor.author Wang, Yang
dc.contributor.author Sahin, Orhan
dc.contributor.author Zhang, Qijing
dc.contributor.department Veterinary Microbiology and Preventive Medicine
dc.date 2018-02-17T11:12:51.000
dc.date.accessioned 2020-07-07T05:14:29Z
dc.date.available 2020-07-07T05:14:29Z
dc.date.copyright Tue Jan 01 00:00:00 UTC 2013
dc.date.issued 2013-03-15
dc.description.abstract <p>Arsenic, a toxic metalloid, exists in the natural environment and its organic form is approved for use as a feed additive for animal production. As a major foodborne pathogen of animal origin,<em>Campylobacter</em> is exposed to arsenic selection pressure in the food animal production environments. Previous studies showed that <em>Campylobacter</em> isolates from poultry were highly resistant to arsenic compounds and a 4-gene operon (containing <em>arsP</em>, <em>arsR</em>, <em>arsC</em>, and <em>acr3</em>) was associated with arsenic resistance in <em>Campylobacter</em>. However, this 4-gene operon is only present in some <em>Campylobacter</em> isolates and other arsenic resistance mechanisms in <em>C. jejuni</em>have not been characterized. In this study, we determined the role of several putative arsenic resistance genes including <em>arsB</em>, <em>arsC2</em>, and <em>arsR3</em> in arsenic resistance in <em>C. jejuni</em> and found that <em>arsB</em>, but not the other two genes, contributes to the resistance to arsenite and arsenate. Inactivation of <em>arsB</em> in <em>C. jejuni</em> resulted in 8- and 4-fold reduction in the MICs of arsenite and arsenate, respectively, and complementation of the <em>arsB</em> mutant restored the MIC of arsenite. Additionally, overexpression of <em>arsB</em> in <em>C. jejuni</em> 11168 resulted in a 16-fold increase in the MIC of arsenite. PCR analysis of <em>C. jejuni</em> isolates from different animals hosts indicated that <em>arsB</em>and <em>acr3</em> (the 4-gene operon) are widely distributed in various <em>C. jejuni</em> strains, suggesting that<em>Campylobacter</em> requires at least one of the two genes for adaptation to arsenic-containing environments. These results identify ArsB as an alternative mechanism for arsenic resistance in<em>C. jejuni</em> and provide new insights into the adaptive mechanisms of <em>Campylobacter</em> in animal food production environments.</p>
dc.description.comments <p>This article is from PLoS ONE 8(3): e58894. doi:<a href="http://dx.doi.org/PLoS%20ONE%208(3):%20e58894.%20doi:10.1371/journal.pone.0058894" target="_blank">10.1371/journal.pone.0058894</a>. Posted with permission.</p>
dc.format.mimetype application/pdf
dc.identifier archive/lib.dr.iastate.edu/vmpm_pubs/131/
dc.identifier.articleid 1128
dc.identifier.contextkey 8049198
dc.identifier.s3bucket isulib-bepress-aws-west
dc.identifier.submissionpath vmpm_pubs/131
dc.identifier.uri https://dr.lib.iastate.edu/handle/20.500.12876/92234
dc.language.iso en
dc.source.bitstream archive/lib.dr.iastate.edu/vmpm_pubs/131/2013_Shen_ContributionArsB.pdf|||Fri Jan 14 19:44:21 UTC 2022
dc.source.uri 10.1371/journal.pone.0058894
dc.subject.disciplines Animal Diseases
dc.subject.disciplines Bacteriology
dc.subject.disciplines Veterinary Infectious Diseases
dc.subject.disciplines Veterinary Microbiology and Immunobiology
dc.subject.disciplines Veterinary Preventive Medicine, Epidemiology, and Public Health
dc.subject.disciplines Veterinary Toxicology and Pharmacology
dc.subject.keywords Arsenic
dc.subject.keywords Arsenates
dc.subject.keywords Campylobacter
dc.subject.keywords Operons
dc.subject.keywords Polymerase chain reaction
dc.subject.keywords Plasmid construction
dc.subject.keywords Poultry
dc.subject.keywords Campylobacter jejuni
dc.title The Contribution of ArsB to Arsenic Resistance in Campylobacter jejuni
dc.type article
dc.type.genre article
dspace.entity.type Publication
relation.isAuthorOfPublication 1c6a5dfc-c604-457f-85be-122910db782e
relation.isOrgUnitOfPublication 16f8e472-b1cd-4d8f-b016-09e96dbc4d83
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