Glucose monitoring in fission yeast via the Gpa2 galpha, the git5 Gbeta and the git3 putative glucose receptor.

Glucose monitoring in fission yeast via the Gpa2 galpha, the git5 Gbeta and the git3 putative glucose receptor.
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通过 Gpa2 galpha、git5 Gbeta 和 git3 假定的葡萄糖受体监测裂殖酵母中的葡萄糖。

DOI:
10.1093/genetics/156.2.513
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发表时间:
2000
期刊:
影响因子:
3.3
通讯作者:
Hoffman,CS
Hoffman,CS
中科院分区:
生物学2区
文献类型:
--
作者:
Welton,RM;Hoffman,CS

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裂殖酵母通过激活腺苷酸环化酶对环境葡萄糖产生反应。产生的cAMP信号激活蛋白激酶A(PKA)。PKA抑制葡萄糖饥饿诱导的过程,如接合和减数分裂,以及编码果糖-1,6-二磷酸酶的fbp 1基因的转录。我们先前鉴定了葡萄糖抑制bp 1转录所需的git基因的集合,包括编码PKA催化亚基的pka 1/git 6,编码腺苷酸环化酶的git 2/git 1,以及腺苷酸环化酶激活所需的六个“上游”基因。git 8基因与gpa 2基因相同,编码异源三聚体鸟嘌呤核苷酸结合蛋白(Gα)的α亚基,而git 5编码Gβ亚基。gpa ~(2+)的多拷贝抑制研究表明S. pombeadenylate环化酶的激活可能类似于哺乳动物II型酶,依次被Gα和βγ激活。我们在这里表明,激活等位基因ofgpa 2(gpa 2 R176 H,携带突变的编码区的GTdR域)完全抑制突变int 3和git 5,导致我们的模型的改进。我们描述了git 3的克隆,并表明它编码一个假定的七跨膜G蛋白偶联受体。Agit 3缺失与PKA途径的其他组分的缺失赋予相同的表型,包括发芽延迟、组成性fbp 1转录和饥饿独立接合。由于git 3的缺失被gpa 2 R176 H等位基因完全抑制,因此git 3似乎编码一个G蛋白偶联葡萄糖受体,负责激活粟酒裂殖酵母中的腺苷酸环化酶。
The fission yeastSchizosaccharomyces pomberesponds to environmental glucose by activating adenylate cyclase. The resulting cAMP signal activates protein kinase A (PKA). PKA inhibits glucose starvation-induced processes, such as conjugation and meiosis, and the transcription of thefbp1gene that encodes the gluconeogenic enzyme fructose-1,6-bisphosphatase. We previously identified a collection ofgitgenes required for glucose repression offbp1transcription, includingpka1/git6, encoding the PKA catalytic subunit,git2/cyr1, encoding adenylate cyclase, and six “upstream” genes required for adenylate cyclase activation. Thegit8gene, identical togpa2, encodes the alpha subunit of a heterotrimeric guanine-nucleotide binding protein (Gα) whilegit5encodes a Gβ subunit. Multicopy suppression studies withgpa2+previously indicated thatS. pombeadenylate cyclase activation may resemble that of the mammalian type II enzyme with sequential activation by Gα followed by βγ. We show here that an activated allele ofgpa2(gpa2R176H, carrying a mutation in the coding region for the GTPase domain) fully suppresses mutations ingit3andgit5, leading to a refinement in our model. We describe the cloning ofgit3and show that it encodes a putative seven-transmembrane G protein-coupled receptor. Agit3deletion confers the same phenotypes as deletions of other components of the PKA pathway, including a germination delay, constitutivefbp1transcription, and starvation-independent conjugation. Since thegit3deletion is fully suppressed by thegpa2R176Hallele with respect tofbp1transcription,git3appears to encode a G protein-coupled glucose receptor responsible for adenylate cyclase activation inS. pombe.
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