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HUMMR, a hypoxia- and HIF-1α–inducible protein, alters mitochondrial distribution and transport
Yan Li1,3, Seung Lim5, David Hoffman4, Pontus Aspenstrom6, Howard J. Federoff5, and David A. Rempe1,2,3
1Department of Neurology, Center for Neural Development and Disease, 2Interdepartmental Graduate Program in Neuroscience, 3Interdepartmental Graduate Program in Biomedical Genetics, and 4Department of Anesthesiology, University of Rochester School of Medicine & Dentistry, Rochester, NY 14642
5Georgetown University Medical Center, Washington, DC 20057
6Department of Microbiology, Tumour and Cell Biology, Karolinska Institute, SE-171 77 Stockholm, Sweden
Mitochondrial transport is critical for maintenance of normal neuronal function. Here, we identify a novel mitochondria protein, hypoxia up-regulated mitochondrial movement regulator (HUMMR), which is expressed in neurons and is markedly induced by hypoxia-inducible factor 1 α (HIF-1α). Interestingly, HUMMR interacts with Miro-1 and Miro-2, mitochondrial proteins that are critical for mediating mitochondrial transport. Interestingly, knockdown of HUMMR or HIF-1 function in neurons exposed to hypoxia markedly reduces mitochondrial content in axons. Because mitochondrial transport and distribution are inextricably linked, the impact of reduced HUMMR function on the direction of mitochondrial transport was also explored. Loss of HUMMR function in hypoxia diminished the percentage of motile mitochondria moving in the anterograde direction and enhanced the percentage moving in the retrograde direction. Thus, HUMMR, a novel mitochondrial protein induced by HIF-1 and hypoxia, biases mitochondria transport in the anterograde direction. These findings have broad implications for maintenance of neuronal viability and function during physiological and pathological states.
