Mitochondrial fission is an acute and adaptive response in injured motor neurons

Sumiko Kiryu-Seo, Hiromi Tamada, Yukina Kato, Katsura Yasuda, Naotada Ishihara, Masatoshi Nomura, Katsuyoshi Mihara, Hiroshi Kiyama

Research output: Contribution to journalArticlepeer-review

40 Citations (Scopus)


Successful recovery from neuronal damage requires a huge energy supply, which is provided by mitochondria. However, the physiological relevance of mitochondrial dynamics in damaged neurons in vivo is poorly understood. To address this issue, we established unique bacterial artificial chromosome transgenic (BAC Tg) mice, which develop and function normally, but in which neuronal injury induces labelling of mitochondria with green fluorescent protein (GFP) and expression of cre recombinase. GFP-labelled mitochondria in BAC Tg mice appear shorter in regenerating motor axons soon after nerve injury compared with mitochondria in non-injured axons, suggesting the importance of increased mitochondrial fission during the early phase of nerve regeneration. Crossing the BAC Tg mice with mice carrying a floxed dynamin-related protein 1 gene (Drp1), which is necessary for mitochondrial fission, ablates mitochondrial fission specifically in injured neurons. Injury-induced Drp1-deficient motor neurons show elongated or abnormally gigantic mitochondria, which have impaired membrane potential and axonal transport velocity during the early phase after injury, and eventually promote neuronal death. Our in vivo data suggest that acute and prominent mitochondrial fission during the early stage after nerve injury is an adaptive response and is involved in the maintenance of mitochondrial and neuronal integrity to prevent neurodegeneration.

Original languageEnglish
Article number28331
JournalScientific reports
Publication statusPublished - Jun 20 2016

All Science Journal Classification (ASJC) codes

  • General


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