The target of rapamycin complex 1 (TORC1) protein kinase is activated by nutrients and controls nutrient uptake via the membrane trafficking of various nutrient permeases. However, its molecular mechanisms remain elusive. Cholesterol (ergosterol in yeast) in conjunction with sphingolipids forms tight-packing microdomains, "lipid rafts", which are critical for intracellular protein sorting. Here we show that a novel target of rapamycin (TOR)-interacting transcriptional activator Vhr2 is required for full expression of some ERG genes for ergosterol biogenesis and for proper sorting of the tryptophan permease Tat2 in budding yeast. Loss of Vhr2 caused sterol biogenesis disturbance and Tat2 missorting. TORC1 activity maintained VHR2 transcript and protein levels, and total sterol levels. Vhr2 was not involved in regulation of the TORC1-downstream protein kinase Npr1, which regulates Tat2 sorting. This study suggests that TORC1 regulates nutrient uptake via sterol biogenesis.

中文翻译：

---

TORC1通过发芽酵母中的新型转录激活因子Vhr2确保Tat2色氨酸通透酶的膜运输。

雷帕霉素复合物1（TORC1）蛋白激酶的靶标被养分激活，并通过各种养分通透酶的膜运输控制养分吸收。但是，其分子机制仍然难以捉摸。胆固醇（酵母中的麦角固醇）与鞘脂结合形成紧密堆积的微区，即“脂筏”，这对于细胞内蛋白质分选至关重要。在这里，我们显示相互作用的雷帕霉素（TOR）的转录激活因子Vhr2的新目标是麦角固醇生物发生的某些ERG基因的完整表达和发芽酵母中色氨酸通透酶Tat2的正确分类所必需的。Vhr2的丢失导致固醇生物发生障碍和Tat2缺失。TORC1活性维持VHR2转录本和蛋白质水平以及总固醇水平。Vhr2没有参与TORC1下游蛋白激酶Npr1的调节，后者调节Tat2的分类。这项研究表明TORC1通过固醇生物发生调节营养吸收。