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dc.contributor.authorSullivan, Matthew J
dc.contributor.authorGoh, Kelvin GK
dc.contributor.authorGosling, Dean
dc.contributor.authorKatupitiya, Lahiru
dc.contributor.authorUlett, Glen C
dc.date.accessioned2021-07-19T01:16:30Z
dc.date.available2021-07-19T01:16:30Z
dc.date.issued2021
dc.identifier.issn0021-9193
dc.identifier.doi10.1128/JB.00315-21
dc.identifier.urihttp://hdl.handle.net/10072/406093
dc.description.abstractBacteria can utilize Copper (Cu) as a trace element to support cellular processes; however, excess Cu can intoxicate bacteria. Here, we characterize the cop operon in group B streptococcus (GBS), and establish its role in evasion of Cu intoxication and the response to Cu stress on virulence. Growth of GBS mutants deficient in either the copA Cu exporter, or the copY repressor, were severely compromised in Cu-stress conditions. GBS survival of Cu stress reflected a mechanism of CopY de-repression of the CopA efflux system. However, neither mutant was attenuated for intracellular survival in macrophages. Analysis of global transcriptional responses to Cu by RNA-sequencing revealed a stress signature encompassing homeostasis of multiple metals. Genes induced by Cu stress included putative metal transporters for manganese import, whereas a system for iron export was repressed. In addition, copA promoted the ability of GBS to colonize the blood, liver and spleen of mice following disseminated infection. Together, these findings show that GBS copA mediates resistance to Cu intoxication, via regulation by the Cu-sensing transcriptional repressor, copY. Cu stress responses in GBS reflect a transcriptional signature that heightens virulence and represents an important part of the bacteria's ability to survive in different environments. Importance: Understanding how bacteria manage cellular levels of metal ions, such as copper, helps to explain how microbial cells can survive in different stressful environments. We show how the opportunistic pathogen group B Streptococcus (GBS) achieves homeostasis of intracellular copper through the activities of the genes that comprise the cop operon, and describe how this helps GBS survive in stressful environments, including in the mammalian host during systemic disseminated infection.
dc.description.peerreviewedYes
dc.languageEnglish
dc.publisherAmerican Society for Microbiology
dc.relation.ispartofpagefrom1
dc.relation.ispartofpageto49
dc.relation.ispartofjournalJournal of Bacteriology
dc.subject.fieldofresearchBiological sciences
dc.subject.fieldofresearchAgricultural, veterinary and food sciences
dc.subject.fieldofresearchBiomedical and clinical sciences
dc.subject.fieldofresearchcode31
dc.subject.fieldofresearchcode30
dc.subject.fieldofresearchcode32
dc.titleCopper intoxication in group B Streptococcus triggers transcriptional activation of the cop operon that contributes to enhanced virulence during acute infection
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationSullivan, MJ; Goh, KGK; Gosling, D; Katupitiya, L; Ulett, GC, Copper intoxication in group B Streptococcus triggers transcriptional activation of the cop operon that contributes to enhanced virulence during acute infection., J Bacteriol, 2021, pp. JB0031521-
dc.date.updated2021-07-19T00:20:57Z
dc.description.versionAccepted Manuscript (AM)
gro.rights.copyright© 2021 American Society for Microbiology. This is the author-manuscript version of this paper. Reproduced in accordance with the copyright policy of the publisher. Please refer to the journal's website for access to the definitive, published version.
gro.hasfulltextFull Text
gro.griffith.authorUlett, Glen C.


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