Skip to main content
  • ASM
    • Antimicrobial Agents and Chemotherapy
    • Applied and Environmental Microbiology
    • Clinical Microbiology Reviews
    • Clinical and Vaccine Immunology
    • EcoSal Plus
    • Eukaryotic Cell
    • Infection and Immunity
    • Journal of Bacteriology
    • Journal of Clinical Microbiology
    • Journal of Microbiology & Biology Education
    • Journal of Virology
    • mBio
    • Microbiology and Molecular Biology Reviews
    • Microbiology Resource Announcements
    • Microbiology Spectrum
    • Molecular and Cellular Biology
    • mSphere
    • mSystems
  • Log in
  • My Cart

Main menu

  • Home
  • Articles
    • Archive
  • About the Journal
    • About EC
    • For Librarians
    • For Advertisers
    • FAQ
  • ASM
    • Antimicrobial Agents and Chemotherapy
    • Applied and Environmental Microbiology
    • Clinical Microbiology Reviews
    • Clinical and Vaccine Immunology
    • EcoSal Plus
    • Eukaryotic Cell
    • Infection and Immunity
    • Journal of Bacteriology
    • Journal of Clinical Microbiology
    • Journal of Microbiology & Biology Education
    • Journal of Virology
    • mBio
    • Microbiology and Molecular Biology Reviews
    • Microbiology Resource Announcements
    • Microbiology Spectrum
    • Molecular and Cellular Biology
    • mSphere
    • mSystems

User menu

  • Log in
  • My Cart

Search

  • Advanced search
Eukaryotic Cell
publisher-logosite-logo

Advanced Search

  • Home
  • Articles
    • Archive
  • About the Journal
    • About EC
    • For Librarians
    • For Advertisers
    • FAQ
Articles

Bcr1 Functions Downstream of Ssd1 To Mediate Antimicrobial Peptide Resistance in Candida albicans

Sook-In Jung, Jonathan S. Finkel, Norma V. Solis, Siyang Chaili, Aaron P. Mitchell, Michael R. Yeaman, Scott G. Filler
Sook-In Jung
Division of Infectious Diseases, Chonnom National University Medical School, Gwangju, South Korea
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Jonathan S. Finkel
Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Norma V. Solis
Division of Infectious Diseases, Harbor-UCLA Medical Center, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, USA
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Siyang Chaili
Division of Infectious Diseases, Harbor-UCLA Medical Center, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, USA
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Aaron P. Mitchell
Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Michael R. Yeaman
Division of Infectious Diseases, Harbor-UCLA Medical Center, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, USADivision of Molecular Medicine, Harbor-UCLA Medical Center, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, USADavid Geffen School of Medicine at UCLA, Los Angeles, California, USA
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Scott G. Filler
Division of Infectious Diseases, Harbor-UCLA Medical Center, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, USADavid Geffen School of Medicine at UCLA, Los Angeles, California, USA
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
DOI: 10.1128/EC.00285-12
  • Article
  • Figures & Data
  • Info & Metrics
  • PDF
Loading

ABSTRACT

In order to colonize the host and cause disease, Candida albicans must avoid being killed by host defense peptides. Previously, we determined that the regulatory protein Ssd1 governs antimicrobial peptide resistance in C. albicans. Here, we sought to identify additional genes whose products govern susceptibility to antimicrobial peptides. We discovered that a bcr1Δ/Δ mutant, like the ssd1Δ/Δ mutant, had increased susceptibility to the antimicrobial peptides, protamine, RP-1, and human β defensin-2. Homozygous deletion of BCR1 in the ssd1Δ/Δ mutant did not result in a further increase in antimicrobial peptide susceptibility. Exposure of the bcr1Δ/Δ and ssd1Δ/Δ mutants to RP-1 induced greater loss of mitochondrial membrane potential and increased plasma membrane permeability than with the control strains. Therefore, Bcr1 and Ssd1 govern antimicrobial peptide susceptibility and likely function in the same pathway. Furthermore, BCR1 mRNA expression was downregulated in the ssd1Δ/Δ mutant, and the forced expression of BCR1 in the ssd1Δ/Δ mutant partially restored antimicrobial peptide resistance. These results suggest that Bcr1 functions downstream of Ssd1. Interestingly, overexpression of 11 known Bcr1 target genes in the bcr1Δ/Δ mutant failed to restore antimicrobial peptide resistance, suggesting that other Bcr1 target genes are likely responsible for antimicrobial peptide resistance. Collectively, these results demonstrate that Bcr1 functions downstream of Ssd1 to govern antimicrobial peptide resistance by maintaining mitochondrial energetics and reducing membrane permeabilization.

FOOTNOTES

    • Received 9 October 2012.
    • Accepted 21 December 2012.
    • Accepted manuscript posted online 11 January 2013.
  • Supplemental material for this article may be found at http://dx.doi.org/10.1128/EC.00285-12.

  • Copyright © 2013, American Society for Microbiology. All Rights Reserved.
View Full Text
PreviousNext
Back to top
Download PDF
Citation Tools
Bcr1 Functions Downstream of Ssd1 To Mediate Antimicrobial Peptide Resistance in Candida albicans
Sook-In Jung, Jonathan S. Finkel, Norma V. Solis, Siyang Chaili, Aaron P. Mitchell, Michael R. Yeaman, Scott G. Filler
Eukaryotic Cell Feb 2013, 12 (3) 411-419; DOI: 10.1128/EC.00285-12

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Print

Email

Thank you for sharing this Eukaryotic Cell article.

NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. We do not retain these email addresses.

Enter multiple addresses on separate lines or separate them with commas.
Bcr1 Functions Downstream of Ssd1 To Mediate Antimicrobial Peptide Resistance in Candida albicans
(Your Name) has forwarded a page to you from Eukaryotic Cell
(Your Name) thought you would be interested in this article in Eukaryotic Cell.
Share
Bcr1 Functions Downstream of Ssd1 To Mediate Antimicrobial Peptide Resistance in Candida albicans
Sook-In Jung, Jonathan S. Finkel, Norma V. Solis, Siyang Chaili, Aaron P. Mitchell, Michael R. Yeaman, Scott G. Filler
Eukaryotic Cell Feb 2013, 12 (3) 411-419; DOI: 10.1128/EC.00285-12
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
  • Top
  • Article
    • ABSTRACT
    • INTRODUCTION
    • MATERIALS AND METHODS
    • RESULTS
    • DISCUSSION
    • ACKNOWLEDGMENTS
    • FOOTNOTES
    • REFERENCES
  • Figures & Data
  • Info & Metrics
  • PDF

Related Articles

Cited By...

About

  • About EC
  • For the Media
  • For Librarians
  • For Advertisers
  • FAQ
  • Permissions
  • Journal Announcements

Authors

  • Submit a Manuscript to mSphere

ASM Journals

ASM journals are the most prominent publications in the field, delivering up-to-date and authoritative coverage of both basic and clinical microbiology.

About ASM | Contact Us | Press Room

 

ASM is a member of

Scientific Society Publisher Alliance

Copyright © 2019 American Society for Microbiology | Privacy Policy | Website feedback

Print ISSN: 1535-9778; Online ISSN: 1535-9786