Cryptococcal cell morphology affects host cell interactions and pathogenicity.
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Cryptococcus neoformans is a common life-threatening human fungal pathogen. The size of cryptococcal cells is typically 5 to 10 microm. Cell enlargement was observed in vivo, producing cells up to 100 microm. These morphological changes in cell size affected pathogenicity via reducing phagocytosis by host mononuclear cells, increasing resistance to oxidative and nitrosative stress, and correlated with reduced penetration of the central nervous system. Cell enlargement was stimulated by coinfection with strains of opposite mating type, and ste3aDelta pheromone receptor mutant strains had reduced cell enlargement. Finally, analysis of DNA content in this novel cell type revealed that these enlarged cells were polyploid, uninucleate, and produced daughter cells in vivo. These results describe a novel mechanism by which C. neoformans evades host phagocytosis to allow survival of a subset of the population at early stages of infection. Thus, morphological changes play unique and specialized roles during infection.
Lung Diseases, Fungal
Mice, Inbred A
Reverse Transcriptase Polymerase Chain Reaction
Published Version (Please cite this version)10.1371/journal.ppat.1000953
Publication InfoOkagaki, Laura H; Strain, Anna K; Nielsen, Judith N; Charlier, Caroline; Baltes, Nicholas J; Chrétien, Fabrice; ... Nielsen, Kirsten (2010). Cryptococcal cell morphology affects host cell interactions and pathogenicity. PLoS Pathog, 6(6). pp. e1000953. 10.1371/journal.ppat.1000953. Retrieved from https://hdl.handle.net/10161/4602.
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Chair, Department of Molecular Genetics and Microbiology
Joseph Heitman was an undergraduate at the University of Chicago (1980-1984), graduating from the BS-MS program with dual degrees in chemistry and biochemistry with general and special honors. He then matriculated as an MD-PhD student at Cornell and Rockefeller Universities and worked with Peter Model and Norton Zinder on how restriction enzymes recognize specific DNA sequences and how bacteria respond to and repair DNA breaks and nicks. Dr. Heitman moved as an EMBO long-term fellow to the Bi
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