Essential amino acids and glutamine regulate induction of mitochondrial elongation during autophagy
Essential amino acids and glutamine regulate induction of mitochondrial elongation during autophagy
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DOI：
10.4161/cc.10.16.17002
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发表时间：
2011-08-15
期刊：
影响因子：
4.3
通讯作者：
Scorrano, Luca
中科院分区：
文献类型：
--
作者：
Gomes, Ligia C.;Di Benedetto, Giulietta;Scorrano, Luca
线粒体形态和超微结构的调节变化调节几个细胞过程，包括凋亡和我们最近描述的自噬。延长的线粒体免于自噬降解，并且具有更多的嵴，其中ATP合酶的活性增加，从而在营养耗尽期间维持ATP水平。最终，线粒体延长对于细胞在大自噬期间的存活至关重要。是否延长是一个普遍的反应，缺乏所有的营养物质，或者如果线粒体不同的反应，存在不同的是不清楚。在这里，我们表明，线粒体形状不同的营养反应：当细胞在氨基酸的存在下，而不是葡萄糖饥饿时，延长被抑制。有趣的是，饥饿诱导的线粒体伸长是一个可逆的过程，但补充氨基酸不足以恢复饥饿后的线粒体形态。复杂的控制途径可能是在适当的位置连接不同能量来源的细胞器的形状。
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.