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首页> 美国卫生研究院文献>G3: GenesGenomesGenetics >Vesicular Trafficking Systems Impact TORC1-Controlled Transcriptional Programs in Saccharomyces cerevisiae
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Vesicular Trafficking Systems Impact TORC1-Controlled Transcriptional Programs in Saccharomyces cerevisiae

机译：泡酒运输系统影响酿酒酵母中TORC1控制的转录程序。

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The Target of Rapamycin Complex I (TORC1) orchestrates global reprogramming of transcriptional programs in response to myriad environmental conditions, yet, despite the commonality of the TORC1 complex components, different TORC1-inhibitory conditions do not elicit a uniform transcriptional response. In Saccharomyces cerevisiae, TORC1 regulates the expression of nitrogen catabolite repressed (NCR) genes by controlling the nuclear translocation of the NCR transactivator Gln3. Moreover, Golgi-to-endosome trafficking was shown to be required for nuclear translocation of Gln3 upon a shift from rich medium to the poor nitrogen source proline, but not upon rapamycin treatment. Here, we employed microarray profiling to survey the full impact of the vesicular trafficking system on yeast TORC1-orchestrated transcriptional programs. In addition to the NCR genes, we found that ribosomal protein, ribosome biogenesis, phosphate-responsive, and sulfur-containing amino acid metabolism genes are perturbed by disruption of Golgi-to-endosome trafficking following a nutritional shift from rich to poor nitrogen source medium, but not upon rapamycin treatment. Similar to Gln3, defects in Golgi-to-endosome trafficking significantly delayed cytoplasmic–nuclear translocation of Sfp1, but did not detectably affect the cytoplasmic–nuclear or nuclear–cytoplasmic translocation of Met4, which are the transactivators of these genes. Thus, Golgi-to-endosome trafficking defects perturb TORC1 transcriptional programs via multiple mechanisms. Our findings further delineate the downstream transcriptional responses of TORC1 inhibition by rapamycin compared with a nitrogen quality downshift. Given the conservation of both TORC1 and endomembrane networks throughout eukaryotes, our findings may also have implications for TORC1-mediated responses to nutritional cues in mammals and other eukaryotes.
机译：雷帕霉素复合物I（TORC1）的目标可响应各种环境条件来协调转录程序的全局重编程，但是，尽管TORC1复合物组件具有共同性，但不同的TORC1抑制条件并不能引起统一的转录反应。在酿酒酵母中，TORC1通过控制NCR反式激活因子Gln3的核转运来调节氮分解代谢物阻抑（NCR）基因的表达。此外，已证明从富培养基向贫氮源脯氨酸转变时，Gln3的核转运需要高尔基体向内体运输，而雷帕霉素治疗则不需要。在这里，我们采用了微阵列分析来调查水泡运输系统对酵母TORC1调控的转录程序的全部影响。除NCR基因外，我们发现核糖体蛋白，核糖体生物发生，磷酸盐反应性和含硫氨基酸代谢基因也受到营养从富氮源向贫氮源转移的高尔基体向内体运输的干扰。 ，但不接受雷帕霉素治疗。与Gln3相似，高尔基体到内体的运输缺陷显着延迟了Sfp1的胞质-核易位，但并未检测到Met4的胞质-核或核-胞质易位，后者是这些基因的反式激活因子。因此，高尔基体到内体的运输缺陷通过多种机制干扰TORC1转录程序。我们的发现进一步描绘了雷帕霉素抑制TORC1的下游转录反应，与氮素质量下降相比。鉴于在整个真核生物中都保留了TORC1和内膜网络，我们的发现也可能对TORC1介导的对哺乳动物和其他真核生物营养线索的反应具有影响。

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