Shipping Calpastatin to the Rescue: Prevention of Neuromuscular Degeneration through Mitofusin 2

Paula Rebelo; Marta Giacomello; Luca Scorrano

doi:10.1016/j.cmet.2018.09.017

Shipping Calpastatin to the Rescue: Prevention of Neuromuscular Degeneration through Mitofusin 2

Cell Metab. 2018 Oct 2;28(4):536-538. doi: 10.1016/j.cmet.2018.09.017.

Authors

Paula Rebelo¹, Marta Giacomello², Luca Scorrano³

Affiliations

¹ Department of Biology, University of Padua, Via U Bassi 58B, 35121 Padua, Italy.
² Department of Biology, University of Padua, Via U Bassi 58B, 35121 Padua, Italy. Electronic address: marta.giacomello@unipd.it.
³ Department of Biology, University of Padua, Via U Bassi 58B, 35121 Padua, Italy; Venetian Institute of Molecular Medicine, Via Orus 2, 35129 Padua, Italy. Electronic address: luca.scorrano@unipd.it.

PMID: 30282045
DOI: 10.1016/j.cmet.2018.09.017

Abstract

How neuromuscular junctions (NMJs) are lost in disease and aging is unclear. Recently in Cell Metabolism, Wang et al. (2018) discovered that endoplasmic reticulum-mitochondria tethering by Mitofusin 2 is required to organize a cleft between these two organelles, which, like a lorry, traffics down the axon to distribute calpastatin to terminals where it blocks NMJ degradation.

Publication types

Research Support, Non-U.S. Gov't
Comment

MeSH terms

Axonal Transport*
Calcium-Binding Proteins
Mitochondria
Muscle, Skeletal
Neuromuscular Junction*

Substances

Calcium-Binding Proteins
calpastatin