G-Protein Coupled Receptor from YeastSaccharomyces cerevisiae

Yun, Cheol Won; Tamaki, Hiroyuki; Nakayama, Reiko; Yamamoto, Kenji; Kumagai, Hidehiko

doi:10.1006/bbrc.1997.7649

Cited by 90 publications

(76 citation statements)

References 12 publications

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“…Gpr1 belongs to the G protein-coupled seven-transmembrane receptor (GPCR) superfamily (Yun et al 1997;Xue et al 1998) and Gpa2 is a member of the heterotrimeric G protein a subunit (G a ) protein family (Nakafuku et al 1988). Addition of glucose to derepressed cells activates Gpr1, which in turn stimulates the exchange of GDP for GTP on Gpa2 (Kraakman et al 1999a).…”

Section: Regulation Of the Camp-pka Pathwaymentioning

confidence: 99%

Life in the midst of scarcity: adaptations to nutrient availability in Saccharomyces cerevisiae

et al. 2010

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Cells of all living organisms contain complex signal transduction networks to ensure that a wide range of physiological properties are properly adapted to the environmental conditions. The fundamental concepts and individual building blocks of these signalling networks are generally well-conserved from yeast to man; yet, the central role that growth factors and hormones play in the regulation of signalling cascades in higher eukaryotes is executed by nutrients in yeast. Several nutrient-controlled pathways, which regulate cell growth and proliferation, metabolism and stress resistance, have been defined in yeast. These pathways are integrated into a signalling network, which ensures that yeast cells enter a quiescent, resting phase (G 0 ) to survive periods of nutrient scarceness and that they rapidly resume growth and cell proliferation when nutrient conditions become favourable again. A series of well-conserved nutrient-sensory protein kinases perform key roles in this signalling network: i.e. Snf1, PKA, Tor1 and Tor2, Sch9 and Pho85-Pho80. In this review, we provide a comprehensive overview on the current understanding of the signalling processes mediated via these kinases with a particular focus on how these individual pathways converge to signalling networks that ultimately ensure the dynamic translation of extracellular nutrient signals into appropriate physiological responses.

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Section: Regulation Of the Camp-pka Pathwaymentioning

confidence: 99%

Life in the midst of scarcity: adaptations to nutrient availability in Saccharomyces cerevisiae

et al. 2010

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“…These issues are beginning to be addressed with the identification of a role for genes such as GPR1 and MEP2 in filamentous growth. GPR1 encodes a Gpa2p-coupled, seven-transmembrane domain receptor and may function to sense extracellular signals and regulate cAMP levels via Gpa2p (Yun et al 1997;Xue et al 1998). The MEP2 gene, encoding a high-affinity ammonium permease, has recently been demonstrated to control filamentous growth, i.e., deletion of MEP2 is sufficient to block filament formation (Lorenz and Heitman 1998).…”

Section: Saccharomyces Cerevisiaementioning

confidence: 99%

Signaling via cAMP in fungi: interconnections with mitogen-activated protein kinase pathways

Kronstad¹,

Maria²,

Funnell³

et al. 1998

Archives of Microbiology

171

102

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“…Upstream of PKA lies Gpr1, a G-protein-coupled receptor that senses glucose. This activates the Rasdependent adenylyl cyclase to produce cAMP production that in turn stimulates the activity of protein kinase A (PKA) (Matsumoto et al 1982;Boutelet et al 1985;Yun et al 1997;Santangelo 2006).…”

mentioning

confidence: 99%

Stb3 Plays a Role in the Glucose-Induced Transition from Quiescence to Growth inSaccharomyces cerevisiae

Liko¹,

Conway

Grunwald

et al. 2010

Genetics

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Addition of glucose to quiescent Saccharomyces cerevisiae cells causes the immediate induction of $1000 genes. These genes include ribosomal proteins (RP) and non-RP genes needed for ribosome production and other growth processes. RRPE sequence elements are commonly found 59 of non-RP growth gene ORFs, and Stb3 has recently been identified as an RRPE binding protein. Stb3 overexpression (Stb3OE) produces a slow growth phenotype that is associated with reduced expression of non-RP genes and a drop in the rate of amino acid incorporation. Genes affected by Stb3 are associated with a TGAAAAA motif. Stb3 is restricted to the nucleus in quiescent cells and is immediately released into the cytoplasm after glucose repletion. The Stb3OE slow growth phenotype is reversed by loss of Hos2 histone deactylase activity, consistent with the idea that repression involves histone deacetylation. SCH9 overexpression or PPH22 deletion, mutations that activate target of rapamycin (Tor) nutrient sensing pathways, also reverse the Stb3OE phenotype. Inhibition of Tor signaling makes the phenotype more severe and restricts Stb3 to the nucleus. The results support a model in which Stb3 is one of the components that repress a large set of growth genes as nutrients are depleted. This repression is ended by glucose.

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G-Protein Coupled Receptor from YeastSaccharomyces cerevisiae

Cited by 90 publications

References 12 publications

Life in the midst of scarcity: adaptations to nutrient availability in Saccharomyces cerevisiae

Life in the midst of scarcity: adaptations to nutrient availability in Saccharomyces cerevisiae

Signaling via cAMP in fungi: interconnections with mitogen-activated protein kinase pathways

Stb3 Plays a Role in the Glucose-Induced Transition from Quiescence to Growth inSaccharomyces cerevisiae

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