Abstract
Besides its role in controlling the morphology of mitochondria, mitofusin-2 has been proposed to tether mitochondria to the endoplasmic reticulum (ER), based largely on light microscopic analysis. In this study we have examined by electron microscopy the organization of ER and mitochondria in cells expressing or not mitofusin-2. Contrary to previous studies, we observed that loss of mitofusin-2 increased ER-mitochondria juxtaposition. These results suggest that mitofusin-2 does not play a critical role in the juxtapostion of ER and mitochondria, and highlight the essential role of ultrastructural analysis to visualize and measure contact between two intracellular compartments.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cells, Cultured
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Cytoplasm / metabolism
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Cytoplasm / ultrastructure*
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Embryo, Mammalian
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Endoplasmic Reticulum / metabolism
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Endoplasmic Reticulum / ultrastructure*
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Fibroblasts / metabolism
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Fibroblasts / ultrastructure*
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GTP Phosphohydrolases / deficiency
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GTP Phosphohydrolases / genetics*
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Gene Knockout Techniques
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Genes, Reporter
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Green Fluorescent Proteins
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Mice
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Microscopy, Electron
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Microscopy, Fluorescence
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Mitochondria / metabolism
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Mitochondria / ultrastructure*
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Transfection
Substances
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Green Fluorescent Proteins
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GTP Phosphohydrolases
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Mfn2 protein, mouse
Grants and funding
This work was supported by a grant from the Swiss National Science Foundation (
http://www.snf.ch/E/Pages/default.aspx) to PC (31003A_135789). The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.