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首页> 外文期刊>Molecular biology of the cell >Trans-Golgi Network and Endosome Dynamics Connect Ceramide Homeostasis with Regulation of the Unfolded Protein Response and TOR Signaling in Yeast
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Trans-Golgi Network and Endosome Dynamics Connect Ceramide Homeostasis with Regulation of the Unfolded Protein Response and TOR Signaling in Yeast

机译：反式高尔基网络和内体动力学连接神经酰胺稳态与酵母中未折叠的蛋白质反应和TOR信号的调节。

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Synthetic genetic array analyses identify powerful genetic interactions between a thermosensitive allele (sec14-1(ts)) of the structural gene for the major yeast phosphatidylinositol transfer protein (SEC14) and a structural gene deletion allele (tlg2 Delta) for the Tlg2 target membrane-soluble N-ethylmaleimide-sensitive factor attachment protein receptor. The data further demonstrate Sec14 is required for proper trans-Golgi network (TGN)/endosomal dynamics in yeast. Paradoxically, combinatorial depletion of Sec14 and Tlg2 activities elicits trafficking defects from the endoplasmic reticulum, and these defects are accompanied by compromise of the unfolded protein response (UPR). UPR failure occurs downstream of Hac1 mRNA splicing, and it is further accompanied by defects in TOR signaling. The data link TGN/endosomal dynamics with ceramide homeostasis, UPR activity, and TOR signaling in yeast, and they identify the Sit4 protein phosphatase as a primary conduit through which ceramides link to the UPR. We suggest combinatorial Sec14/Tlg2 dysfunction evokes inappropriate turnover of complex sphingolipids in endosomes. One result of this turnover is potentiation of ceramide-activated phosphatase-mediated down-regulation of the UPR. These results provide new insight into Sec14 function, and they emphasize the TGN/endosomal system as a central hub for homeostatic regulation in eukaryotes.
机译：合成遗传阵列分析确定了主要酵母磷脂酰肌醇转移蛋白（SEC14）的结构基因的热敏等位基因（sec14-1（ts））与Tlg2目标膜的结构基因缺失等位基因（tlg2 Delta）之间的强大遗传相互作用。可溶性N-乙基马来酰亚胺敏感因子附着蛋白受体。数据进一步表明，Sec14是酵母中正确的反高尔基网络（TGN）/内体动力学所必需的。矛盾的是，Sec14和Tlg2活性的组合消耗会引起内质网的运输缺陷，并且这些缺陷会伴随着未折叠蛋白反应（UPR）的破坏。 UPR失败发生在Hac1 mRNA剪接的下游，并且还伴有TOR信号缺陷。数据将TGN /内体动力学与酵母中的神经酰胺稳态，UPR活性和TOR信号联系起来，他们确定Sit4蛋白磷酸酶是神经酰胺与UPR连接的主要途径。我们建议组合Sec14 / Tlg2功能障碍引起内体中复杂鞘脂的不适当更新。这种转换的结果是增强了神经酰胺激活的磷酸酶介导的UPR下调。这些结果提供了对Sec14功能的新见解，并强调了TGN /内体系统是真核生物体内稳态调节的中心枢纽。

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