Franzot SP, Doering TL Inositol acylation of glycosylphosphatidylinositols in the pathogenic fungus Cryptococcus neoformans and the model yeast Saccharomyces cerevisiae Biochemical Journal (1999)
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Journal NLM ID:2984726R WWW link:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1220218/ Publisher: London, UK : Published by Portland Press on behalf of the Biochemical Society Correspondence: tdoeringmail.med.cornell.edu Institutions: Department of Pharmacology, LC-218, Cornell University Medical College, 1300 York Avenue, New York, NY 10021, USA
Cryptococcus neoformans, an opportunistic fungus responsible for life-threatening infection in immunocompromised patients, is able to synthesize glycosylphosphatidylinositol (GPI) structures. Radiolabelling experiments in vitro with the use of a cryptococcal cell-free system showed that the pathway begins as in other eukaryotes, with the addition of N-acetylglucosamine to phosphatidylinositol, followed by deacetylation of the sugar residue. The third step, acylation of the inositol ring, seemed to involve a fatty acid other than palmitate, in contrast with previous findings in Saccharomyces cerevisiae and mammalian GPI pathways. A systematic study of inositol acylation in C. neoformans and S. cerevisiae showed that both organisms used a variety of fatty acids in this step; these were transferred directly from acyl-CoA to inositol without modification. However, the specificity of fatty acid utilization was quite distinct in the two fungi, with the pathogen being substantially more restrictive. In mammalian cells fatty acids added exogenously as acyl-CoAs are not transferred directly to inositol. These results suggest significant differences in the GPI biosynthetic pathway between mammalian and C. neoformans cells that could represent targets for anti-cryptococcal therapy.
Methods: TLC, radiolabeling, enzymatic digestion Synthetic data: synthesis Comments, role: cell-free in vitro data on glycosylphosphatidylinositol synthesis are present in the paper
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