Work

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

Year: 2014

Type: article

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.

Source: The Journal of Cell Biology

DOI: 10.1083/jcb.201306121

Authors: Valentina Debattisti, Diana Pendin, Elena Ziviani, Andrea Daga, Luca Scorrano

Institutions: Veneto Institute of Molecular Medicine, Dulbecco Telethon Institute, IRCCS Eugenio Medea, University of Geneva, University of Padua

Language: English

Topic: Mitochondrial Function and Pathology

Subfield: Molecular Biology

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: hybrid

OpenAlex ID: W2077906609