The Flagellar Transcriptional Regulator FtcR Controls Brucella melitensis 16M Biofilm Formation via a betI-Mediated Pathway in Response to Hyperosmotic Stress

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dc.citation.issue17
dc.citation.volume23
dc.contributor.authorGuo J
dc.contributor.authorDeng X
dc.contributor.authorZhang Y
dc.contributor.authorSong S
dc.contributor.authorZhao T
dc.contributor.authorZhu D
dc.contributor.authorCao S
dc.contributor.authorBaryshnikov PI
dc.contributor.authorCao G
dc.contributor.authorBlair HT
dc.contributor.authorChen C
dc.contributor.authorGu X
dc.contributor.authorLiu L
dc.contributor.authorZhang H
dc.coverage.spatialSwitzerland
dc.date.accessioned2024-01-04T01:35:53Z
dc.date.accessioned2024-07-25T06:37:58Z
dc.date.available2022-08-31
dc.date.available2024-01-04T01:35:53Z
dc.date.available2024-07-25T06:37:58Z
dc.date.issued2022-09
dc.description.abstractThe expression of flagellar proteins in Brucella species likely evolved through genetic transference from other microorganisms, and contributed to virulence, adaptability, and biofilm formation. Despite significant progress in defining the molecular mechanisms behind flagellar gene expression, the genetic program controlling biofilm formation remains unclear. The flagellar transcriptional factor (FtcR) is a master regulator of the flagellar system’s expression, and is critical for B. melitensis 16M’s flagellar biogenesis and virulence. Here, we demonstrate that FtcR mediates biofilm formation under hyperosmotic stress. Chromatin immunoprecipitation with next-generation sequencing for FtcR and RNA sequencing of ftcR-mutant and wild-type strains revealed a core set of FtcR target genes. We identified a novel FtcR-binding site in the promoter region of the osmotic-stress-response regulator gene betI, which is important for the survival of B. melitensis 16M under hyperosmotic stress. Strikingly, this site autoregulates its expression to benefit biofilm bacteria’s survival under hyperosmotic stress. Moreover, biofilm reduction in ftcR mutants is independent of the flagellar target gene fliF. Collectively, our study provides new insights into the extent and functionality of flagellar-related transcriptional networks in biofilm formation, and presents phenotypic and evolutionary adaptations that alter the regulation of B. melitensis 16M to confer increased tolerance to hyperosmotic stress.
dc.format.pagination9905-
dc.identifier.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/36077302
dc.identifier.citationGuo J, Deng X, Zhang Y, Song S, Zhao T, Zhu D, Cao S, Baryshnikov PI, Cao G, Blair HT, Chen C, Gu X, Liu L, Zhang H. (2022). The Flagellar Transcriptional Regulator FtcR Controls Brucella melitensis 16M Biofilm Formation via a betI-Mediated Pathway in Response to Hyperosmotic Stress.. Int J Mol Sci. 23. 17. (pp. 9905-).
dc.identifier.doi10.3390/ijms23179905
dc.identifier.eissn1422-0067
dc.identifier.elements-typejournal-article
dc.identifier.issn1661-6596
dc.identifier.piiijms23179905
dc.identifier.urihttps://mro.massey.ac.nz/handle/10179/70583
dc.languageeng
dc.publisherMDPI (Basel, Switzerland)
dc.relation.isPartOfInt J Mol Sci
dc.rights(c) The authoren
dc.rights.licenseCC BY 4.0en
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/en
dc.subjectBrucella melitensis 16M
dc.subjectbetI
dc.subjectbiofilm
dc.subjectflagellar transcriptional factor FtcR
dc.subjecthyperosmotic stress
dc.subjectBacterial Proteins
dc.subjectBiofilms
dc.subjectBrucella melitensis
dc.subjectBrucellosis
dc.subjectGene Expression Regulation, Bacterial
dc.subjectHumans
dc.subjectTranscription Factors
dc.subjectVirulence
dc.titleThe Flagellar Transcriptional Regulator FtcR Controls Brucella melitensis 16M Biofilm Formation via a betI-Mediated Pathway in Response to Hyperosmotic Stress
dc.typeJournal article
pubs.elements-id455761
pubs.organisational-groupOther
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