The human fungal pathogen, Candida albicans, is very proficient at several classical virulence factors such as morphogenesis, adhesion, biofilm formation and immune evasion through β-glucan masking. The protein kinase A (PKA) pathway is involved in both morphogenesis and β-glucan masking. Several signals converge onto the PKA pathway, but it contains only a single upstream G-protein coupled receptor, Gpr1. We identified specific residues within the N-terminal tail of Gpr1 that are required for methionine-induced morphogenesis through Tpk2. Furthermore, we observe that Gpr1-Gpa2 has an active role in exposing glucans. Even though Gpr1 is required for survival when C. albicans is challenged with macrophages, specifically disrupting morphogenesis did not attenuate this survival. Additionally, constitutive The human fungal pathogen, Candida albicans, is very proficient at several classical virulence factors such as morphogenesis, adhesion, biofilm formation and immune evasion through β-glucan masking. The protein kinase A (PKA) pathway is involved in both morphogenesis and β-glucan masking. Several signals converge onto the PKA pathway, but it contains only a single upstream G-protein coupled receptor, Gpr1. We identified specific residues within the N-terminal tail of Gpr1 that are required for methionine-induced morphogenesis through Tpk2. Furthermore, we observe that Gpr1-Gpa2 has an active role in exposing glucans. Even though Gpr1 is required for survival when C. albicans is challenged with macrophages, specifically disrupting morphogenesis did not attenuate this survival. Additionally, constitutive β-glucan masking did not improve C. albicans survival rates in the macrophage assay. Taken together, this indicates that Gpr1 may regulate additional mechanisms, possibly through glutamine 461, which are crucial in a macrophage context. β-glucan masking did not improve C. albicans survival rates in the macrophage assay. Taken together, this indicates that Gpr1 may regulate additional mechanisms, possibly through glutamine 461, which are crucial in a macrophage context.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.