albicans Sur7p paralog Fmp45p, in the presence of high salt (1.0 M NaCl) in both the SUR7 + and SUR7 – strains. Thus the cellular localization and increased fluorescence intensities suggest that Fmp45p may play a role in survival at high temperature and salt conditions in the sur7Δ mutant. This suggests

functional similarities learn more between SUR7 and FMP45 that are important for growth and survival in more extreme environmental conditions. We have so far been unsuccessful in our efforts to generate a C. albicans sur7Δ fmp45Δ null mutant, and it remains to be determined if these genes are synthetic lethal in C. albicans. There is limited data on the role of endocytosis in Candida pathogenesis. Previously, C. albicans ORFs homologous to S. cerevisiae endocytosis genes were investigated for their involvement in polarized cell growth [32]. Specifically, the authors examined ABP1, BZZ1, EDE1, and PAN1, whose gene products are involved in the early stages of endocytosis [33]. Loss of function of PAN1, but not ABP1,

BZZ1, or EDE1, resulted this website in altered hyphal formation [32]. More recently, Douglas et al [34] investigated the role of C. albicans RVS161 and RVS167 whose homologues in S. cerevisiae are involved in the severance of budding endocytic vesicles from the plasma membrane. Deletion of these genes resulted in strains that produced aberrant filamentous structures and exhibited decreased virulence in a mouse model of disseminated candidiasis [34]. In S. cerevisiae, SUR7 localizes to eisosomes which are immobile protein assemblies that mark sites on the plasma click here membrane for endocytosis [3]. Defective endocytosis as a result of the deletion of SUR7 in C. albicans has been described for the yeast form of this important pathogen [2]. However, the role of C. albicans SUR7 in pathogenesis has not been previously examined. We present here results of experiments whose main focus was to characterize the Glutathione peroxidase structural and physiologic role of C. albicans SUR7, in order to provide a foundation to understanding the role of SUR7 in pathogenesis. Thus, we next turned our attention to assessing the functional

contribution of C. albicans SUR7 to several key virulence-related attributes. The C. albicans sur7Δ mutant was delayed in filamentation when induced on solid media, although this overall defect was minor. Microscopic examination revealed that the sur7Δ filaments branched extensively, and ultrastructurally contained subcellular structures resembling those seen in the C. albicans sur7Δ yeast cells. Alvarez et al. [2] also describe pseudohyphal growth of the sur7Δ mutant strain including an apparent defect in cell polarization, as evidenced by weak filipin staining. However, it is not clear why C. albicans SUR7 affects Sap or lipase secretion, as there is currently little known of the role of endocytosis in the secretion of Saps, lipases, and phospholipases. Importantly, the C.