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Regulation of mitochondrial plasticity by the i-AAA protease YME1L
Biological Chemistry ( IF 3.7 ) Pub Date : 2020-05-26 , DOI: 10.1515/hsz-2020-0120
Yohsuke Ohba 1 , Thomas MacVicar 1 , Thomas Langer 1, 2
Affiliation  

Abstract Mitochondria are multifaceted metabolic organelles and adapt dynamically to various developmental transitions and environmental challenges. The metabolic flexibility of mitochondria is provided by alterations in the mitochondrial proteome and is tightly coupled to changes in the shape of mitochondria. Mitochondrial proteases are emerging as important posttranslational regulators of mitochondrial plasticity. The i-AAA protease YME1L, an ATP-dependent proteolytic complex in the mitochondrial inner membrane, coordinates mitochondrial biogenesis and dynamics with the metabolic output of mitochondria. mTORC1-dependent lipid signaling drives proteolytic rewiring of mitochondria by YME1L. While the tissue-specific loss of YME1L in mice is associated with heart failure, disturbed eye development, and axonal degeneration in the spinal cord, YME1L activity supports growth of pancreatic ductal adenocarcinoma cells. YME1L thus represents a key regulatory protease determining mitochondrial plasticity and metabolic reprogramming and is emerging as a promising therapeutic target.

中文翻译:

i-AAA 蛋白酶 YME1L 对线粒体可塑性的调节

摘要 线粒体是多方面的代谢细胞器,动态适应各种发育转变和环境挑战。线粒体的代谢灵活性是由线粒体蛋白质组的改变提供的,并且与线粒体形状的变化密切相关。线粒体蛋白酶正在成为线粒体可塑性的重要翻译后调节剂。i-AAA 蛋白酶 YME1L 是线粒体内膜中一种 ATP 依赖性蛋白水解复合物,可将线粒体生物发生和动力学与线粒体的代谢输出相协调。mTORC1 依赖性脂质信号驱动 YME1L 对线粒体的蛋白水解重新布线。虽然小鼠中 YME1L 的组织特异性缺失与心力衰竭、眼睛发育障碍和脊髓轴索变性有关,YME1L 活性支持胰腺导管腺癌细胞的生长。因此,YME1L 代表了一种决定线粒体可塑性和代谢重编程的关键调节蛋白酶,并且正在成为一个有希望的治疗靶点。
更新日期:2020-05-26
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