Translational regulation of mitochondrial biogenesis.
Translational regulation of mitochondrial biogenesis.
复制标题
DOI：
10.1042/bst20160071c
复制
发表时间：
2016-12
影响因子：
3.9
通讯作者：
Yi Zhang;Hong Xu
中科院分区：
文献类型：
--
作者：
Yi Zhang;Hong Xu
线粒体是由核基因组和线粒体基因组上的基因表达产生的。线粒体的生物合成是高度可塑性的细胞能量需求，发育信号和环境刺激。雷帕霉素机制靶点（mTOR）通路调节线粒体生物合成，以协调能量稳态与细胞生长。线粒体蛋白在外膜上的局部翻译促进了它们的有效输入，从而在细胞快速生长和增殖期间允许惊人的线粒体生物合成。我们推测，本地翻译也可能允许细胞促进线粒体生物合成选择性的基础上，个别细胞器的健身。MDI-Larp复合物促进健康线粒体的生物合成，从而对于健康线粒体的选择性传递是必不可少的。另一方面，PTEN诱导的推定激酶1（PINK 1）-Pakin激活受损线粒体上的蛋白质合成，以维持细胞器的稳态和活性。本文还对miRNAs调控线粒体生物合成的研究进展进行了综述。
Mitochondria are generated by the expression of genes on both nuclear and mitochondrial genome. Mitochondrial biogenesis is highly plastic in response to cellular energy demand, developmental signals and environmental stimuli. Mechanistic target of rapamycin (mTOR) pathway regulates mitochondrial biogenesis to co-ordinate energy homeostasis with cell growth. The local translation of mitochondrial proteins on the outer membrane facilitates their efficient import and thereby allows prodigious mitochondrial biogenesis during rapid cell growth and proliferation. We postulate that the local translation may also allow cells to promote mitochondrial biogenesis selectively based on the fitness of individual organelle. MDI-Larp complex promotes the biogenesis of healthy mitochondria and thereby is essential for the selective transmission of healthy mitochondria. On the other hand, PTEN-induced putative kinase 1 (PINK1)-Pakin activates protein synthesis on damaged mitochondria to maintain the organelle homeostasis and activity. We also summarize some recent progress on miRNAs' regulation on mitochondrial biogenesis.