The Fission Yeast git5 Gene Encodes a Gβ Subunit Required for Glucose-Triggered Adenylate Cyclase Activation
| Autor: | Charles S. Hoffman, Sheila Landry, Maria T. Pettit, Ethel Apolinario |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
G protein
Protein subunit Molecular Sequence Data DNA Recombinant GTP-Binding Protein beta Subunits Adenylate kinase Biology Cyclase Open Reading Frames Heterotrimeric G protein Schizosaccharomyces Cyclic AMP Genetics heterocyclic compounds Amino Acid Sequence Cloning Molecular Codon Derepression DNA Primers Base Sequence Sequence Homology Amino Acid fungi Heterotrimeric GTP-Binding Proteins Enzyme Activation G beta-gamma complex Glucose Phenotype Biochemistry Schizosaccharomyces pombe Proteins Adenylyl Cyclases Research Article |
| Zdroj: | Europe PubMed Central |
| ISSN: | 1943-2631 |
| DOI: | 10.1093/genetics/154.4.1463 |
| Popis: | Fission yeast adenylate cyclase is activated by the gpa2 Gα subunit of a heterotrimeric guanine-nucleotide binding protein (G protein). We show that the git5 gene, also required for this activation, encodes a Gβ subunit. In contrast to another study, we show that git5 is not a negative regulator of the gpa1 Gα involved in the pheromone response pathway. While 43% identical to mammalian Gβ's, the git5 protein lacks the amino-terminal coiled-coil found in other Gβ subunits, yet the gene possesses some of the coding capacity for this structure 5′ to its ORF. Although both gpa2 (Gα) and git5 (Gβ) are required for adenylate cyclase activation, only gpa2 is needed to maintain basal cAMP levels. Strains bearing a git5 disruption are derepressed for fbp1 transcription and sexual development even while growing in a glucose-rich environment, although fbp1 derepression is half that observed in gpa2 deletion strains. Multicopy gpa2 partially suppresses the loss of git5, while the converse is not true. These data suggest that Gβ is required for activation of adenylate cyclase either by promoting the activation of Gα or by independently activating adenylate cyclase subsequent to Gα stimulation as seen in type II mammalian adenylate cyclase activation. |
| Databáze: | OpenAIRE |
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