Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Alerts
  • Advertising/recruitment
  • Subscribe
  • Contact
  • Current Issue
  • Past Issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • 100th Anniversary of Insulin's Discovery (Jan 2021)
    • Hypoxia-inducible factors in disease pathophysiology and therapeutics (Oct 2020)
    • Latency in Infectious Disease (Jul 2020)
    • Immunotherapy in Hematological Cancers (Apr 2020)
    • Big Data's Future in Medicine (Feb 2020)
    • Mechanisms Underlying the Metabolic Syndrome (Oct 2019)
    • Reparative Immunology (Jul 2019)
    • View all review series ...
  • Viewpoint
  • Collections
    • Recently published
    • In-Press Preview
    • Commentaries
    • Concise Communication
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • Recently published
  • In-Press Preview
  • Commentaries
  • Concise Communication
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Alerts
  • Advertising/recruitment
  • Subscribe
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a letter
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need Help? E-mail the JCI
  • Top
  • Version history
  • Article usage
  • Citations to this article

Advertisement

CorrigendumMicrobiology Free access | 10.1172/JCI27890C1

Glucosylceramide synthase is an essential regulator of pathogenicity of Cryptococcus neoformans

Philipp C. Rittershaus, Talar B. Kechichian, Jeremy C. Allegood, Alfred H. Merrill, Mirko Hennig, Chiara Luberto, and Maurizio Del Poeta

Find articles by Rittershaus, P. in: JCI | PubMed | Google Scholar

Find articles by Kechichian, T. in: JCI | PubMed | Google Scholar

Find articles by Allegood, J. in: JCI | PubMed | Google Scholar

Find articles by Merrill, A. in: JCI | PubMed | Google Scholar

Find articles by Hennig, M. in: JCI | PubMed | Google Scholar

Find articles by Luberto, C. in: JCI | PubMed | Google Scholar

Find articles by Del Poeta, M. in: JCI | PubMed | Google Scholar

Published May 1, 2007 - More info

Published in Volume 117, Issue 5 on May 1, 2007
J Clin Invest. 2007;117(5):1450–1450. https://doi.org/10.1172/JCI27890C1.
© 2007 The American Society for Clinical Investigation
Published May 1, 2007 - Version history
View PDF

Related article:

Glucosylceramide synthase is an essential regulator of pathogenicity of Cryptococcus neoformans
Philipp C. Rittershaus, … , Chiara Luberto, Maurizio Del Poeta
Philipp C. Rittershaus, … , Chiara Luberto, Maurizio Del Poeta
Research Article Microbiology

Glucosylceramide synthase is an essential regulator of pathogenicity of Cryptococcus neoformans

  • Text
  • PDF
Abstract

The pathogenic fungus Cryptococcus neoformans infects humans upon inhalation and causes the most common fungal meningoencephalitis in immunocompromised subjects worldwide. In the host, C. neoformans is found both intracellularly and extracellularly, but how these two components contribute to the development of the disease is largely unknown. Here we show that the glycosphingolipid glucosylceramide (GlcCer), which is present in C. neoformans, was essential for fungal growth in host extracellular environments, such as in alveolar spaces and in the bloodstream, which are characterized by a neutral/alkaline pH, but not in the host intracellular environment, such as in the phagolysosome of macrophages, which is characteristically acidic. Indeed, a C. neoformans mutant strain lacking GlcCer did not grow in vitro at a neutral/alkaline pH, yet it had no growth defect at an acidic pH. The mechanism by which GlcCer regulates alkali tolerance was by allowing the transition of C. neoformans through the cell cycle. This study establishes C. neoformans GlcCer as a key virulence factor of cryptococcal pathogenicity, with important implications for future development of new antifungal strategies.

Authors

Philipp C. Rittershaus, Talar B. Kechichian, Jeremy C. Allegood, Alfred H. Merrill, Mirko Hennig, Chiara Luberto, Maurizio Del Poeta

×

Original citation: J. Clin. Invest.116:1651-1659 (2006). doi:10.1172/JCI27890.

Citation for this corrigendum: J. Clin. Invest.117:1450 (2007). doi:10.1172/JCI27890C1.

During the preparation of the manuscript, an error was introduced in Results and in the Figure 2 legend. The fatty acid attached to the ceramide backbone of glucosylceramide at m/z 756.7 was given incorrectly. The correct fatty acid is hydroxy-C18:0.

The authors regret this error.

Version history
  • Version 1 (May 1, 2007): No description

Article tools

  • View PDF
  • Download citation information
  • Send a letter
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need Help? E-mail the JCI

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Version history
Advertisement
Advertisement
Follow JCI:
Copyright © 2021 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts