Cover image of the article: Role of N-Acetylglucosamine in Ca2+ and Mg2+ ions- regulated Fila- mentous Growth and Protein Glycosylation in C. albicans

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Role of N-Acetylglucosamine in Ca2+ and Mg2+ ions- regulated Fila- mentous Growth and Protein Glycosylation in C. albicans

Authors

M ER-RASFA1,*
1Associate Professor, Laboratory of Pharmacology, Faculty of medicine and pharmacy, University of sidi Mohamed Ben Abdellah, Fez, Morocco
*Corresponding Author: Laboratoire de Pharmacologie, Facult de Mdecine et de Pharmacie, Universit Sidi Mohamed Ben Abdellah, Fez, 30000, Morocco, pharmacologiefmpf@yahoo.fr. Tel: +212-35619320. Fax: +212-35619321. Email: pharmacologiefmpf@yahoo.fr

Shiraz E-Medical Journal:Vol. 9, issue 2; 57-67
Published online:Apr 01, 2008
Article type:Research Article
Received:Sep 19, 2007
Accepted:Feb 15, 2008
How to Cite:ER-RASFA M. Role of N-Acetylglucosamine in Ca2+ and Mg2+ ions- regulated Fila- mentous Growth and Protein Glycosylation in C. albicans. Shiraz E-Med J. 2008;9(2):. doi:

Abstract

Glucose or N-Acetylglucosamine induce similar filamentous growth and a specific calcium and magnesium-dependent intracellular glycoprotein pattern in C. albicans at 37 C in vitro. Both filament growth and its associated glycoprotein pattern are inhibited by calcium ions. The above inhibition can be reversed by magnesium ions, though only in N-Acetylglucosamine- but not in glucose-treated cells. Our data show that in contrast to glucose, N-Acetylglucosamine more than being only a carbon source, it is a key factor for filamentous growth and intracellu- lar protein glycosylation to occur, and thus, it may effect the interaction of C. albicans with its host in a calcium- and magnesium-dependent manner.

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© 2008, Author(s). This open-access article is available under the Creative Commons Attribution 4.0 (CC BY 4.0) International License (https://creativecommons.org/licenses/by/4.0/), which allows for unrestricted use, distribution, and reproduction in any medium, provided that the original work is properly cited.

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