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Proc. Natl. Acad. Sci. USA, First published July 22, 2019 | https://doi.org/10.1073/pnas.1818830116 Increased ER–mitochondria tethering promotes axon regeneration

Soyeon Lee^a,b, Wei Wang^a,b,1, Jinyeon Hwang^c, Uk Namgung^c, and Kyung-Tai Min^a,b,2

^aDepartment of Biological Sciences, School of Life Sciences, Ulsan National Institute of Science and Technology, 44919 Ulsan, South Korea;^b National Creative Research Initiative Center for Proteostasis, Ulsan National Institute of Science and Technology, 44919 Ulsan, South Korea; and ^cDepartment of Oriental Medicine, Daejeon University, 34520 Daejeon, South Korea

¹ Present address: School of Mental Health, Wen Zhou Medical University, 325035 Wen Zhou, Zhejiang Province, China.
²To whom correspondence may be addressed.

Abstract

Translocation of the endoplasmic reticulum (ER) and mitochondria to the site of axon injury has been shown to facilitate axonal regeneration; however, the existence and physiological importance of ER–mitochondria tethering in the injured axons are unknown. Here, we show that a protein linking ER to mitochondria, the glucose regulated protein 75 (Grp75), is locally translated at axon injury site following axotomy, and that overexpression of Grp75 in primary neurons increases ER–mitochondria tethering to promote regrowth of injured axons. We find that increased ER–mitochondria tethering elevates mitochondrial Ca ²⁺ and enhances ATP generation, thereby promoting regrowth of injured axons. Furthermore, intrathecal delivery of lentiviral vector encoding Grp75 to an animal with sciatic nerve crush injury enhances axonal regeneration and functional recovery. Together, our findings suggest that increased ER–mitochondria tethering at axonal injury sites may provide a therapeutic strategy for axon regeneration.

axon regeneration, mitochondria, ER

논문정보

형식Research article
게재일2019년 07월 (BRIC 등록일 2019-07-30)
연구진국내 연구진
분야 생명과학 > 세포생물학

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