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We developed a precision chemoptogenetic approach to target neuronal mitochondria in the intact nervous system in vivo. MG2I, a chemical fluorogen, produces singlet oxygen when bound to the fluorogen-activating protein dL5** and exposed to far-red light. Transgenic zebrafish expressing dL5** within neuronal mitochondria showed dramatic MG2I- and light-dependent neurobehavioral deficits, caused by neuronal bioenergetic crisis and acute neuronal depolarization. These abnormalities resulted from loss of neuronal respiration, associated with mitochondrial fragmentation, swelling and elimination of cristae. Remaining cellular ultrastructure was preserved initially, but cellular pathology downstream of mitochondrial damage eventually culminated in neuronal death. Our work provides powerful new chemoptogenetic tools for investigating mitochondrial homeostasis and pathophysiology and shows a direct relationship between mitochondrial function, neuronal biogenetics and whole-animal behavior.<\/jats:p>","DOI":"10.7554\/elife.51845","type":"journal-article","created":{"date-parts":[[2020,3,16]],"date-time":"2020-03-16T20:00:21Z","timestamp":1584388821000},"source":"Crossref","is-referenced-by-count":25,"title":["Chemoptogenetic ablation of neuronal mitochondria in vivo with spatiotemporal precision and controllable severity"],"prefix":"10.7554","volume":"9","author":[{"given":"Wenting","family":"Xie","sequence":"first","affiliation":[{"name":"Department of Neurology, University of Pittsburgh, Pittsburgh, United States"},{"name":"Pittsburgh Institute for Neurodegenerative Diseases, University of Pittsburgh, Pittsburgh, United States"},{"name":"Tsinghua University Medical School, Beijing, 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