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New mutations of Saccharomyces cerevisiae that partially relieve both glucose and galactose repression activate the protein kinase Snf1

机译:酿酒酵母的新突变可部分缓解葡萄糖和半乳糖的抑制,从而激活蛋白激酶Snf1

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摘要

We isolated from Saccharomyces cerevisiae two mutants, esc1-1 and ESC3-1, in which genes FBP1, ICL1 or GDH2 were partially derepressed during growth in glucose or galactose. The isolation was done starting with a triple mutant pyc1 pyc2 mth1 unable to grow in glucose ammonium medium and selecting for mutants able to grow in the non-permissive medium. HXT1 and HXT2 which encode glucose transporters were expressed at high glucose concentrations in both esc1-1 and ESC3-1 mutants, while derepression of invertase at low glucose concentrations was impaired. REG1, cloned as a suppressor of ESC3-1, was not allelic to ESC3-1. Two-hybrid analysis showed an increased interaction of the protein kinase Snf1 with Snf4 in the ESC3-1 mutant; this was not due to mutations in SNF1 or SNF4. ESC3-1 did not bypass the requirement of Snf1 for derepression. We hypothesize that ESC3-1 either facilitates activation of Snf1 or interferes with its glucose-dependent inactivation.
机译:我们从酿酒酵母中分离出两个突变体esc1-1和ESC3-1,其中基因FBP1,ICL1或GDH2在葡萄糖或半乳糖的生长过程中被部分抑制。从无法在葡萄糖铵培养基中生长的三重突变体pyc1 pyc2 mth1开始进行分离,然后选择能够在非允许培养基中生长的突变体。编码葡萄糖转运蛋白的HXT1和HXT2在esc1-1和ESC3-1突变体中都以高葡萄糖浓度表达,而在低葡萄糖浓度下的转化酶抑制则受损。克隆为ESC3-1抑制剂的REG1与ESC3-1没有等位基因。两杂交分析表明,在ESC3-1突变体中,蛋白激酶Snf1与Snf4的相互作用增加;这不是由于SNF1或SNF4的突变。 ESC3-1并未绕过Snf1的降压要求。我们假设ESC3-1促进Snf1的激活或干扰其葡萄糖依赖性失活。

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