Abstract
Mitochondria are membrane-bound organelles that power up chemical reactions inside cells through ATP production. Mitochondrial function crucially depends on their morphology, which is dynamically regulated by constant fission and fusion. Hyperfused mitochondria are observed in various diseases, including optic atrophy spectrum disorder. A whole-exome sequence experiment revealed that optic atrophy spectrum disorder involves mutation of SLC25A46, a gene that encodes a mitochondrial outer membrane protein. Knockout of SLC25A46 in cells results in hyperfused mitochondria and a significant reduction in oxygen consumption and ATP production. We developed an opsin-free optogenetic system that enables precise control of mitochondrial fission through induction of mitochondrial-lysosomal contact. Optical stimulation reduces hypefused mitochondria and increases the oxygen consumption rate and ATP production in SLC25A46 knockout cells. These results could inspire new treatment strategies for mitochondrial disease through dynamic control of mitochondrial morphology.
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