Essential amino acids and glutamine regulate induction of mitochondrial elongation during autophagy

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.