期刊
CELL REPORTS
卷 24, 期 9, 页码 2432-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2018.07.088
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资金
- University of New Mexico Center for Spatiotemporal Modeling of Cell Signaling (STMC) [NIH P50GM085273, R01AI116894]
- STMC
- NIH T32 training grant [NIH T32 AI007538]
- Quillen College of Medicine, East Tennessee State University, through NIH [GMR01053522, GMR01119197, GMR01083016, R15AI109581, C06RR030651]
Cell wall mannans of Candida albicans mask beta-(1,3)-glucan from recognition by Dectin-1, contributing to innate immune evasion. Glucan exposures are predominantly single receptor-ligand interaction sites of nanoscale dimensions. Candida species vary in basal glucan exposure and molecular complexity of mannans. We used super-resolution fluorescence imaging and a series of protein mannosylation mutants in C. albicans and C. glabrata to investigate the role of specific N-mannan features in regulating the nanoscale geometry of glucan exposure. Decreasing acid labile mannan abundance and alpha-(1,6)-mannan backbone length correlated most strongly with increased density and nanoscopic size of glucan exposures in C. albicans and C. glabrata, respectively. Additionally, a C. albicans clinical isolate with high glucan exposure produced similarly perturbed N-mannan structures and elevated glucan exposure geometry. Thus, acid labile mannan structure influences the nanoscale features of glucan exposure, impacting the nature of the pathogenic surface that triggers immunoreceptor engagement, aggregation, and signaling.
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