Published in

Rockefeller University Press, Journal of Cell Biology, 3(204), p. 303-312, 2014

DOI: 10.1083/jcb.201306121

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Reduction of endoplasmic reticulum stress attenuates the defects caused by Drosophila mitofusin depletion

Journal article published in 2014 by Valentina Debattisti, Diana Pendin ORCID, Elena Ziviani ORCID, Andrea Daga ORCID, Luca Scorrano
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

Ablation of the mitochondrial fusion and endoplasmic reticulum (ER)–tethering protein Mfn2 causes ER stress, but whether this is just an epiphenomenon of mitochondrial dysfunction or a contributor to the phenotypes in mitofusin (Mfn)-depleted Drosophila melanogaster is unclear. In this paper, we show that reduction of ER dysfunction ameliorates the functional and developmental defects of flies lacking the single Mfn mitochondrial assembly regulatory factor (Marf). Ubiquitous or neuron- and muscle-specific Marf ablation was lethal, altering mitochondrial and ER morphology and triggering ER stress that was conversely absent in flies lacking the fusion protein optic atrophy 1. Expression of Mfn2 and ER stress reduction in flies lacking Marf corrected ER shape, attenuating the developmental and motor defects. Thus, ER stress is a targetable pathogenetic component of the phenotypes caused by Drosophila Mfn ablation.