Canada Research Chair in Mitochondrial Signaling and Physiopathology, Moncton, NB, Canada.
Department of Biology, University of Moncton, Moncton, NB, Canada.
Cell Mol Life Sci. 2022 May 30;79(6):327. doi: 10.1007/s00018-022-04325-y.
The architecture of mitochondria adapts to physiological contexts: while mitochondrial fragmentation is usually associated to quality control and cell death, mitochondrial elongation often enhances cell survival during stress. Understanding how these events are regulated is important to elucidate how mitochondrial dynamics control cell fate. Here, we show that the tyrosine kinase Src regulates mitochondrial morphology. Deletion of Src increased mitochondrial size and reduced cellular respiration independently of mitochondrial mass, mitochondrial membrane potential or ATP levels. Re-expression of Src targeted to the mitochondrial matrix, but not of Src targeted to the plasma membrane, rescued mitochondrial morphology in a kinase activity-dependent manner. These findings highlight a novel function for Src in the control of mitochondrial dynamics.
虽然线粒体碎片化通常与质量控制和细胞死亡有关,但线粒体伸长通常在应激时增强细胞存活。了解这些事件如何被调控对于阐明线粒体动力学如何控制细胞命运非常重要。在这里,我们表明酪氨酸激酶Src 调节线粒体形态。Src 的缺失增加了线粒体的大小并减少了细胞呼吸,而与线粒体质量、线粒体膜电位或 ATP 水平无关。Src 靶向线粒体基质的再表达,而不是 Src 靶向质膜的再表达,以激酶活性依赖的方式挽救了线粒体形态。这些发现强调了 Src 在控制线粒体动力学中的新功能。