ASM conference on Candida and Candidiasis edition:8 location:Denver, USA date:12-17 March 2006
We and others (Maidan, et al., 2005; Miwa, et al., 2004) previously identified the putative G-protein coupled receptor Gpr1 in Candida albicans. The interaction between the G-protein Gpa2 and Gpr1 was clearly established by two-hybrid experiment, and the overactivation of Gpa2 (Gpa2Q354L) does rescue wild type phenotypes in a gpr1 deleted strain. However, neither deletion of Gpa2 or Gpr1 lead to reduced PKA activity. For instance, cAMP induction in response to glucose addition to deprived cells seems independent of the GPCR complex. Similarly, trehalose mobilisation after addition of glucose (downstream process resulting from PKA activation) is not impaired in both mutants. The Gpr1 ligand remains to be identified. Internalisation of Gpr1-GFP fusion in C.albicans is induced by amino acids rather than by glucose, and yet cAMP induction by amino acids is not clearly established, nor it differs between a wild type strain and a gpr1 deleted strain. Gpr1 putatively transmits nutrient-availability signals to other cascades. We therefore aim to identify downstream targets of Gpr1 signalling. The signalling through PKA and the activation of Gpr1 by its ligand may not systematically linked. We are currently performing complementation experiments in yeast to perhaps separate both processes.
Maidan, M.M., et al. (2005) Mol.Biol.Cell 16: 1971-86
Miwa, T., et al. (2004) Eukaryot.Cell 3 : 919-31.