Sasaki Kanae, Yoshida Hiderou
Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo, Hyogo 678-1297, Japan.
Department of Molecular Biochemistry, Graduate School of Life Science, University of Hyogo, Hyogo 678-1297, Japan
J Biochem. 2015 Apr;157(4):185-95. doi: 10.1093/jb/mvv010. Epub 2015 Feb 4.
Organelle autoregulation is a homeostatic mechanism to regulate the capacity of each organelle according to cellular demands. The endoplasmic reticulum (ER) stress response increases the expression of ER chaperones and ER-associated degradation factors when the capacity of the ER becomes insufficient, e.g. during cellular differentiation or viral propagation, and which can be restored through increased synthesis of secretory or membrane proteins. In the Golgi stress response, insufficient organelle capacity is responded to by augmentation of glycosylation enzyme expression and vesicular transport components. The mitochondrial stress response upregulates mitochondrial chaperone and protease expression in the mitochondrial matrix and intermembrane space when unfolded proteins accumulate in the mitochondria. The lysosome stress response is activated during autophagy to enhance the function of the lysosome by transcriptional induction of lysosome genes including cathepsins. However, many of the molecular mechanisms of organelle autoregulation remain unclear. Here, we review recent discoveries in organelle autoregulation and their molecular mechanisms.
细胞器自调节是一种根据细胞需求调节每个细胞器功能的稳态机制。当内质网（ER）的功能变得不足时，例如在细胞分化或病毒繁殖期间，内质网应激反应会增加内质网伴侣蛋白和内质网相关降解因子的表达，并且可以通过增加分泌蛋白或膜蛋白的合成来恢复。在高尔基体应激反应中，细胞器功能不足会通过增加糖基化酶表达和囊泡运输成分来应对。当未折叠蛋白在线粒体中积累时，线粒体应激反应会上调线粒体基质和膜间隙中线粒体伴侣蛋白和蛋白酶的表达。自噬过程中溶酶体应激反应被激活，通过转录诱导包括组织蛋白酶在内的溶酶体基因来增强溶酶体的功能。然而，细胞器自调节的许多分子机制仍不清楚。在这里，我们综述了细胞器自调节及其分子机制的最新发现。
