Rodríguez Cristina, Sanz Pascual, Gancedo Carlos
Instituto de Investigaciones Biomédicas 'Alberto Sols' CSIC-UAM, Unidad de Bioquímica y Genética de Levaduras, C/Arturo Duperier 4, 28029, Madrid, Spain.
FEMS Yeast Res. 2003 Mar;3(1):77-84. doi: 10.1111/j.1567-1364.2003.tb00141.x.
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.
我们从酿酒酵母中分离出了两个突变体esc1-1和ESC3-1，在葡萄糖或半乳糖培养基中生长时，FBP1、ICL1或GDH2基因在这两个突变体中部分去阻遏。分离过程始于一个无法在葡萄糖-铵培养基中生长的三突变体pyc1 pyc2 mth1，并筛选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突变体的高葡萄糖浓度下均有高表达，而在低葡萄糖浓度下转化酶的去阻遏受到损害。作为ESC3-1的抑制子被克隆的REG1与ESC3-1不是等位基因。双杂交分析表明，在ESC3-1突变体中蛋白激酶Snf1与Snf4的相互作用增强；这并非由于SNF1或SNF4中的突变所致。ESC3-1并未绕过Snf1对去阻遏的需求。我们推测ESC3-1要么促进Snf1的激活，要么干扰其葡萄糖依赖性失活。
