Glucose depletion rapidly inhibits translation initiation in yeast
Glucose depletion rapidly inhibits translation initiation in yeast
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DOI：
10.1091/mbc.11.3.833
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发表时间：
2000-03-01
影响因子：
3.3
通讯作者：
Sachs, AB
中科院分区：
文献类型：
--
作者：
Ashe, MP;De Long, SK;Sachs, AB
葡萄糖在酿酒酵母中起着关键的信号分子作用。众所周知，葡萄糖耗竭通过在转录水平上导致基因去抑制的途径来调节基因的表达。在这项研究中，我们研究了葡萄糖耗竭对蛋白质合成的影响。我们发现，从生长介质中撤除葡萄糖会导致蛋白质合成的快速抑制，并且当重新加入葡萄糖时，Mis效应很容易被逆转。无论是抑制还是重新激活翻译都不需要新的转录。这种抑制也不需要激活氨基酸饥饿途径或失活TOR激酶途径。然而，葡萄糖抑制(REG1、glc7、hkx2和ssn6)、己糖转运体诱导(SNF3rgt2)和cAMP依赖的蛋白激酶(tpk1(W)和tpk2(W))途径中的突变对停糖对翻译的抑制作用具有抵抗力。这些发现突显了细胞的营养状态与其翻译能力之间的密切联系。它们还有助于定义酵母转录后调控的新领域。
Glucose performs key functions as a signaling molecule in the yeast Saccharomyces cerevisiae. Glucose depletion is known to regulate gene expression via pathways that lead to derepression of genes at the transcriptional level. in this study, we have investigated the effect of glucose depletion on protein synthesis. We discovered that glucose withdrawal from the growth medium led to a rapid inhibition of protein synthesis and that Mis effect was readily reversed upon readdition of glucose. Neither the inhibition nor the reactivation of translation required new transcription. This inhibition also did not require activation of the amino acid starvation pathway or inactivation of the TOR kinase pathway. However, mutants in the glucose repression (reg1, glc7, hkx2, and ssn6), hexose transporter induction (snf3 rgt2), and cAMP-dependent protein kinase (tpk1(w) and tpk2(w)) pathways were resistant to the inhibitory effects of glucose withdrawal on translation. These findings highlight the intimate connection between the nutrient status of the cell and its translational capacity. They also help to define a new area of posttranscriptional regulation in yeast.