Gene Ontology annotation through association of InterPro records with GO terms
Use of the ND evidence code for Gene Ontology (GO) terms
Annotation inferences using phylogenetic trees
Combined Automated Annotation using Multiple IEA Methods
Candida albicans Pde1p and Gpa2p comprise a regulatory module mediating agonist-induced cAMP signalling and environmental adaptation.
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Gpa2 drives intracellular-acidification-induced cAMP signalling.
"Our biochemical evidence shows that Gpa2 stimulates cAMP signalling in response to intracellular acidification"
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Pde1, not Pde2, terminates glucose- and acidification-induced cAMP signalling.
"Pde1, but not Pde2, is responsible for down-regulation of cAMP signalling induced by glucose addition or intracellular acidification"
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PDE1-GPA2 synthetic growth, morphogenesis and stress defects are interpreted as Gpa2 acting outside the cAMP pathway.
"suggesting that Gpa2 mediates its effects on these processes in a cAMP pathway-independent manner"
A Candida albicans cyclic nucleotide phosphodiesterase: cloning and expression in Saccharomyces cerevisiae and biochemical characterization of the recombinant enzyme.
The PDE1-encoded low-affinity phosphodiesterase in the yeast Saccharomyces cerevisiae has a specific function in controlling agonist-induced cAMP signaling.
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S. cerevisiae Pde1, but not Pde2, limits agonist-induced cAMP accumulation.
"We show that deletion of PDE1, but not PDE2, results in a much higher cAMP accumulation upon addition of glucose or upon intracellular acidification."
The cAMP phosphodiesterase encoded by CaPDE2 is required for hyphal development in Candida albicans.
Farnesol and dodecanol effects on the Candida albicans Ras1-cAMP signalling pathway and the regulation of morphogenesis.
Multiple roles and diverse regulation of the Ras/cAMP/protein kinase A pathway in Candida albicans.
Gpr1, a putative G-protein-coupled receptor, regulates morphogenesis and hypha formation in the pathogenic fungus Candida albicans.
The G protein-coupled receptor Gpr1 and the Galpha protein Gpa2 act through the cAMP-protein kinase A pathway to induce morphogenesis in Candida albicans.
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Glucose-induced cAMP signalling in C. albicans depends on Cdc25-Ras1, not Gpr1-Gpa2.
"deletion of neither CaGpr1 nor CaGpa2 affects glucose-induced cAMP signaling. In contrast, the latter is abolished in strains lacking CaCdc25 or CaRas1, suggesting that the CaCdc25-CaRas1 rather than the CaGpr1-CaGpa2 module mediates glucose-induced cAMP signaling"
Sugar Sensing and Signaling in Candida albicans and Candida glabrata.
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CaGpr1 ligands appear to be lactate and methionine, not sugars.
"However, it seems that the ligand(s) for CaGpr1 are not sugars but lactate and methionine."
Gpa2, a G-protein alpha subunit required for hyphal development in Candida albicans.
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gpa2 filamentation defect is not rescued by cAMP but is bypassed by HST7 (MAPK) overexpression.
"These defects cannot be reversed by exogenous addition of cyclic AMP. However, overexpression of HST7, which encodes a component of the filament-inducing mitogen-activated protein kinase (MAPK) cascade, bypasses the Gpa2 requirement."
Falcon deep research for C. albicans PDE1
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pde1 single mutant filaments normally (citing Inglis & Sherlock 2013 review).
"reports that a **pde1 mutant filaments normally** in the assessed conditions"
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Glucose-induced cAMP in C. albicans requires Cdc25/Ras1, not Gpr1/Gpa2.
"A **2005** *C. albicans* genetic study found that loss of **Gpr1 or Gpa2 did not abolish glucose-induced cAMP signaling**, whereas loss of **Cdc25 or Ras1 did**."
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Recombinant Pde1 is ~13.6-fold more catalytically efficient on cAMP than cGMP (from Hoyer 1994 Vmax values).
"cAMP has approximately 13.6-fold greater *V*max/*K*ₘ"
Carbon source induced yeast-to-hypha transition in Candida albicans is dependent on the presence of amino acids and on the G-protein-coupled receptor Gpr1.
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The physiological ligand of CaGpr1 (sugar vs methionine) is unresolved.
"it remains unclear whether Gpr1 senses sugars, as in Saccharomyces cerevisiae, or specific amino acids like methionine"
OpenScientist hypothesis run: PDE1 and the glucose-activated GPCR pathway (GO:0110034)
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Pde1 terminates the glucose-induced cAMP rise, but the glucose-activated GPCR specification is not supported in C. albicans; GO:1902660 recommended instead.
"prefer GO:1902660 (glucose-mediated signaling) without the GPCR qualifier"