內科CHEN, YEE-CHUNYEE-CHUNCHEN2008-12-292018-07-112008-12-292018-07-112002http://ntur.lib.ntu.edu.tw//handle/246246/95206Filamentation and adherence to host cells are critical virulence factors of Candida albicans . Multiple filamentation regulatory pathways have been discovered in C. albicans using Saccharomyces cerevisiae as a model. In S . cerevisiae , these pathways converge on Flo11p, which functions as a downstream effector of filamentation and also mediates cell-cell adherence (flocculation). In C. albicans , such effector(s) have not yet been identified. Here, we demonstrate that the cell surface protein Als1p is an effector of filamentation in C. albicans . We show that Als1 p expression is controlled by the transcription factor Efg1 p, which is known to be a key regulator of filamentation in C. albicans . Further, disruption of ALS 1 inhibited filamentation, and autonomous expression of Als1p restored filamentation in an efg1 homozygous null mutant. Thus, Als1p functions as a downstream effector of the EFG1 filamentation pathway. In addition, we found that Als1p mediates both flocculation and adherence of C. albicans to endothelial cells in vitro . As a cell surface glycoprotein that mediates filamentation and adherence, Als1p has both structural and functional similarity to S. cerevisiae Flo11p . Consistent with our in vitro results, Als1p was required for both normal filamentation and virulence in the mouse model of haematogenously disseminated candidiasis.en-USCELL-CELL ADHESIONHYPHAL FORMATIONGENEVIRULENCEGROWTHYEASTjournal article