Enjalbert Brice, Parrou Jean Luc, Vincent Olivier, François Jean
Centre de Bioingénierie Gilbert Durand, UMR-CNRS 5504, UR-INRA 792, Département de Génie Biochimique et Alimentaire, Complexe Scientifique de Rangueil, 31077 Toulouse, France1.
Microbiology (Reading). 2000 Oct;146 ( Pt 10):2685-2694. doi: 10.1099/00221287-146-10-2685.
Mutant strains of Saccharomyces cerevisiae defective in respiration have been reported to be unable to store glycogen, as revealed by the iodine-staining method. In this report, it is shown that in contrast to this claim, mitochondrial respiratory mutants accumulated even more glycogen than wild-type cells during the fermentative growth on glucose. However, as soon as glucose was exhausted in the medium, these mutants readily and completely mobilized their glycogen content, contrary to wild-type cells which only transiently degraded this polymer. The mobilization of glycogen was a specific trait resulting from a defect in mitochondrial function that could not be suppressed by mutations in the cAMP- and Pho85 protein kinase-dependent nutrient-sensing pathways, and by other mutations which favour glycogen synthesis. To account for this mobilization, it was found that respiration-defective cells not only contained a less active glycogen synthase, but also a more active glycogen phosphorylase. Since glucose 6-phosphate (Glc6P) is a potent inhibitor of the phosphorylation and an activator of the dephosphorylation processes of glycogen synthase and glycogen phosphorylase, it is suggested that the drop in Glc6P observed at the onset of glucose depletion in respiration-deficient cells triggers this rapid and sustained glycogen mobilization. It is also proposed that this degradation provides the energy for the viability of respiratory mutants in glucose-starved medium.
据报道，通过碘染色法显示，呼吸缺陷型酿酒酵母突变株无法储存糖原。在本报告中，结果表明，与这一说法相反，在以葡萄糖为发酵底物生长期间，线粒体呼吸突变株积累的糖原甚至比野生型细胞更多。然而，一旦培养基中的葡萄糖耗尽，与仅短暂降解这种聚合物的野生型细胞相反，这些突变株会迅速且完全地动用其糖原储备。糖原的动用是线粒体功能缺陷导致的一个特异性特征，不能被cAMP和Pho85蛋白激酶依赖性营养感知途径中的突变以及其他有利于糖原合成的突变所抑制。为了解释这种动用现象，研究发现呼吸缺陷型细胞不仅糖原合酶活性较低，而且糖原磷酸化酶活性较高。由于6-磷酸葡萄糖（Glc6P）是糖原合酶磷酸化过程的有效抑制剂和糖原磷酸化酶去磷酸化过程的激活剂，因此有人认为，在呼吸缺陷型细胞中，葡萄糖耗尽开始时观察到的Glc6P下降引发了这种快速且持续的糖原动用。还提出这种降解为葡萄糖饥饿培养基中呼吸突变株的存活提供了能量。
