Dulbecco-Telethon Institute, Padova, Italy.
Cell Cycle. 2011 Aug 15;10(16):2635-9. doi: 10.4161/cc.10.16.17002.
Regulated changes in mitochondrial morphology and ultrastructure regulate several cellular processes, including apoptosis and, as we recently described, autophagy. Elongated mitochondria are spared from autophagic degradation and possess more cristae, where activity of the ATP synthase is increased, maintaining ATP levels in periods of nutrient depletion. Ultimately, mitochondrial elongation is crucial for cell survival during macroautophagy. Whether elongation is a widespread response to the lack of all nutrients, or if mitochondria respond differently to the presence of different ones is unclear. Here we show that mitochondrial shape responds differently to nutrients: elongation is inhibited when cells are starved in the presence of amino acids but not of glucose. Interestingly, starvation-induced mitochondrial elongation is a reversible process, but replenishment of amino acids is not sufficient to recover mitochondrial morphology after starvation. Intricate control pathways are likely to be in place to connect shape of the organelle with different energetic sources.
线粒体形态和超微结构的调节变化可调控多种细胞过程,包括细胞凋亡,以及我们最近描述的自噬。延长的线粒体免于自噬降解,并具有更多嵴,其中 ATP 合酶的活性增加,在营养物质耗尽期间维持 ATP 水平。最终,线粒体延长对于巨自噬期间的细胞存活至关重要。线粒体延长是否是对所有营养物质缺乏的普遍反应,或者线粒体对不同营养物质的反应是否不同尚不清楚。在这里,我们表明线粒体形状对营养物质的反应不同:当细胞在存在氨基酸的情况下饥饿时,线粒体伸长被抑制,但不存在葡萄糖时则不会。有趣的是,饥饿诱导的线粒体伸长是一个可逆的过程,但在饥饿后补充氨基酸不足以恢复线粒体形态。可能存在复杂的控制途径将细胞器的形状与不同的能量来源联系起来。