Copper sensing transcription factor ArsR2 regulates VjbR to sustain virulence in Brucella abortus .

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  • Additional Information
    • Source:
      Publisher: Taylor & Francis Country of Publication: United States NLM ID: 101594885 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2222-1751 (Electronic) Linking ISSN: 22221751 NLM ISO Abbreviation: Emerg Microbes Infect Subsets: MEDLINE
    • Publication Information:
      Publication: 2019- : [Philadelphia, PA] : Taylor & Francis
      Original Publication: New York : NPG, 2012-2018.
    • Subject Terms:
      Brucella abortus*/genetics ; Brucella abortus*/pathogenicity ; Brucella abortus*/metabolism ; Gene Expression Regulation, Bacterial* ; Copper*/metabolism ; Bacterial Proteins*/genetics ; Bacterial Proteins*/metabolism ; Brucellosis*/microbiology ; Transcription Factors*/genetics ; Transcription Factors*/metabolism; Animals ; Virulence ; Mice ; Female ; Mice, Inbred BALB C ; Type IV Secretion Systems/genetics ; Type IV Secretion Systems/metabolism ; Virulence Factors/genetics ; Virulence Factors/metabolism ; Humans
    • Abstract:
      Brucellosis, caused by the intracellular pathogen Brucella , is a major zoonotic infection that promotes reproductive disease in domestic animals and chronic debilitating conditions in humans. The ArsR family of transcriptional regulators plays key roles in diverse cellular processes, including metal ion homeostasis, responding to adverse conditions, and virulence. However, little is known about the function of ArsR family members in Brucella . Here, we identified ArsR2 as a nonclassical member of the family that lacks autoregulatory function, but which nevertheless plays a vital role in maintaining copper homeostasis in B. abortus . ArsR2 is a global regulator of 241 genes, including those involved in the VirB type IV secretion system (T4SS). Significantly, ArsR2 regulates T4SS production in B. abortus by targeting VjbR which encodes a LuxR-type family transcriptional regulator. Moreover, copper modulates transcriptional activity of ArsR2, but not of VjbR. Furthermore, deletion of arsR2 attenuated virulence in a mouse model. Collectively, these findings enhance understanding of the mechanism by which ArsR proteins regulate virulence gene expression in pathogenic Brucella species.
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    • Contributed Indexing:
      Keywords: ArsR; Brucella; T4SS; VjbR; virulence
    • Accession Number:
      789U1901C5 (Copper)
      0 (Bacterial Proteins)
      0 (Transcription Factors)
      0 (Type IV Secretion Systems)
      0 (Virulence Factors)
    • Publication Date:
      Date Created: 20240919 Date Completed: 20240925 Latest Revision: 20240928
    • Publication Date:
      20240928
    • Accession Number:
      PMC11425708
    • Accession Number:
      10.1080/22221751.2024.2406274
    • Accession Number:
      39295505