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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

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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
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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

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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.

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