Characterization of glycogen-deficient glc mutants of Saccharomyces cerevisiae.
Characterization of glycogen-deficient glc mutants of Saccharomyces cerevisiae.
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DOI：
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发表时间：
1994-02
期刊：
影响因子：
3.3
通讯作者：
J. Cannon;J. Pringle;A. Fiechter;M. Khalil
中科院分区：
文献类型：
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作者：
J. Cannon;J. Pringle;A. Fiechter;M. Khalil
分离到48株糖原代谢缺陷的酿酒酵母突变体。突变确定了8个GLC基因，并确定了其功能。这些基因中的三个突变通过破坏RAS gtpase激活蛋白（GLC1/IRA1和GLC4/IRA2）或激活Ras2p （GLC5/RAS2）激活RAS/cAMP途径。发现SNF1蛋白激酶（GLC2）是正常糖原水平所必需的。糖原分支酶（GLC3）被发现是糖原合成所必需的。GLC6被证明是CIF1（可能还有FDP1、BYP1和GGS1）的等位基因，这些突变先前被发现可以阻止葡萄糖的生长；该基因也与TPS1相同，TPS1编码海藻糖-磷酸盐合成酶的一个亚基。GLC6突变能够增加或降低糖原水平，至少部分是通过影响糖原合成酶的调节。GLC7编码1型蛋白磷酸酶，该酶有助于糖原合成酶的去磷酸化（并因此激活）。GLC8编码1型蛋白磷酸酶抑制剂-2的同源物。明确了GLC1/IRA1、GLC3、GLC4/IRA2、GLC6/CIF1/TPS1（及其相邻的VAT2/VMA2）和GLC7的遗传图谱位置。从GLC3的数据来看，至少在某些菌株中，在染色体V着丝粒附近可能存在重组抑制。
Forty-eight mutants of Saccharomyces cerevisiae with defects in glycogen metabolism were isolated. The mutations defined eight GLC genes, the function of which were determined. Mutations in three of these genes activate the RAS/cAMP pathway either by impairment of a RAS GTPase-activating protein (GLC1/IRA1 and GLC4/IRA2) or by activating Ras2p (GLC5/RAS2). SNF1 protein kinase (GLC2) was found to be required for normal glycogen levels. Glycogen branching enzyme (GLC3) was found to be required for significant glycogen synthesis. GLC6 was shown to be allelic to CIF1 (and probably FDP1, BYP1 and GGS1), mutations in which were previously found to prevent growth on glucose; this gene is also the same as TPS1, which encodes a subunit of the trehalose-phosphate synthase. Mutations in GLC6 were capable of increasing or decreasing glycogen levels, at least in part via effects on the regulation of glycogen synthase. GLC7 encodes a type 1 protein phosphatase that contributes to the dephosphorylation (and hence activation) of glycogen synthase. GLC8 encodes a homologue of type 1 protein phosphatase inhibitor-2. The genetic map positions of GLC1/IRA1, GLC3, GLC4/IRA2, GLC6/CIF1/TPS1 (and the adjacent VAT2/VMA2), and GLC7 were clarified. From the data on GLC3, there may be a suppression of recombination near the chromosome V centromere, at least in some strains.