a Cellular and Molecular Physiology, Institute of Translational Medicine, University of Liverpool , Liverpool , UK.
Autophagy. 2019 Sep;15(9):1634-1637. doi: 10.1080/15548627.2019.1615304. Epub 2019 Jun 9.
Mitochondria and peroxisomes have a number of features in common: they each play interconnected roles in fatty acid and reactive oxygen species (ROS) metabolism and, once damaged, need to be removed by specialized autophagic mechanisms, termed mitophagy and pexophagy, respectively. Both processes can use ubiquitin as an initiating signal but whereas mitophagy has been extensively studied, pexophagy remains rather poorly understood. Our recent work, along with a new study from Kim and colleagues, has shed light on the molecular mechanism of pexophagy and the importance of reversible ubiquitination in its regulation. Collectively, these studies highlight the physiological role of the deubiquitinase USP30 in suppressing the turnover of peroxisomes. : ROS: reactive oxygen species; DUB: deubiquitinase or deubiquitylase; USP: ubiquitin specific protease; PINK1: PTEN induced kinase 1; CAT: catalase; KO: knock-out; SQSTM1/p62: sequestosome 1; LIR: LC3 interacting region; GFP: green fluorescent protein; RFP: red fluorescent protein; CRISPR: Clustered Regularly Interspaced Short Palendromic Repeat.
它们在脂肪酸和活性氧(ROS)代谢中都发挥着相互关联的作用,一旦受损,就需要通过专门的自噬机制(分别称为线粒体自噬和过氧化物酶体自噬)来清除。这两个过程都可以使用泛素作为起始信号,但尽管线粒体自噬已经得到了广泛的研究,而过氧化物酶体自噬仍然知之甚少。我们最近的工作,以及 Kim 及其同事的一项新研究,揭示了过氧化物酶体自噬的分子机制以及其调节中可逆泛素化的重要性。总的来说,这些研究强调了去泛素酶 USP30 在抑制过氧化物酶体周转中的生理作用。ROS:活性氧;DUB:去泛素酶或去泛素化酶;USP:泛素特异性蛋白酶;PINK1:PTEN 诱导的激酶 1;CAT:过氧化氢酶;KO:敲除;SQSTM1/p62:自噬体 1;LIR:LC3 相互作用区域;GFP:绿色荧光蛋白;RFP:红色荧光蛋白;CRISPR:簇状规律间隔短回文重复。