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A non-canonical unfolded protein response pathway and mitochondrial dynamics control the number of ER-mitochondria contact sites

Rieko Kojima, Yuriko Kakimoto, Manatsu Shinmyo, Kazuo Kurokawa, Akihiko Nakano, Toshiya Endo, View ORCID ProfileYasushi Tamura
doi: https://doi.org/10.1101/684753
Rieko Kojima
1Faculty of Science, Yamagata University, 1-4-12 Kojirakawa-machi, Yamagata 990-8560, Japan
2Toyama Prefectural Institute for Pharmaceutical Research, 17-1 Nakataikouyama, Imizu, Toyama 939-0363, Japan
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Yuriko Kakimoto
3Department of Biochemistry and Molecular Biology, Graduate School of Medical Science, Yamagata University, 2-2-2 Iidanishi, Yamagata, 990-9585, Japan
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Manatsu Shinmyo
1Faculty of Science, Yamagata University, 1-4-12 Kojirakawa-machi, Yamagata 990-8560, Japan
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Kazuo Kurokawa
4Live Cell Super-Resolution Imaging Research Team, RIKEN Center for Advanced Photonics, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan
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Akihiko Nakano
4Live Cell Super-Resolution Imaging Research Team, RIKEN Center for Advanced Photonics, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan
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Toshiya Endo
5Faculty of Life Sciences, Kyoto Sangyo University, Kamigamo-motoyama, Kita-ku, Kyoto 603-8555, Japan
6Institute for Protein Dynamics, Kyoto Sangyo University, Kamigamo-motoyama, Kita-ku, Kyoto 603-8555, Japan
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Yasushi Tamura
1Faculty of Science, Yamagata University, 1-4-12 Kojirakawa-machi, Yamagata 990-8560, Japan
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  • ORCID record for Yasushi Tamura
  • For correspondence: tamura@sci.kj.yamagata-u.ac.jp
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Abstract

Mitochondria maintain their morphology and functions through the optimized balance between the mitochondrial fusion and division. Here we report a novel role of mitochondrial dynamics in controlling the number of ER-mitochondria encounter structure (ERMES) clusters in a yeast cell. Loss of mitochondrial fusion or division caused the increased or decreased number, respectively, of ERMES foci observed in cells. ERMES complexes, therefore, appear to cluster with each other and mitochondrial division may inhibit undesired ERMES hyper-clustering. Furthermore, our microscopic analyses suggest that ER stress induces dissociation of ERMES clusters, increasing the number of ERMES foci even in the absence of Ire1 and Hac1, which are essential factors for the UPR response. Interestingly, we found that ER stress leads to expansion of both the ER and mitochondrial membranes in an ERMES function-dependent manner. These findings imply that a cell is equipped with two independent regulatory mechanisms controlling the number of ER-mitochondria contact sites to meet the cellular as well as environmental demands.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted June 27, 2019.
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A non-canonical unfolded protein response pathway and mitochondrial dynamics control the number of ER-mitochondria contact sites
Rieko Kojima, Yuriko Kakimoto, Manatsu Shinmyo, Kazuo Kurokawa, Akihiko Nakano, Toshiya Endo, Yasushi Tamura
bioRxiv 684753; doi: https://doi.org/10.1101/684753
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A non-canonical unfolded protein response pathway and mitochondrial dynamics control the number of ER-mitochondria contact sites
Rieko Kojima, Yuriko Kakimoto, Manatsu Shinmyo, Kazuo Kurokawa, Akihiko Nakano, Toshiya Endo, Yasushi Tamura
bioRxiv 684753; doi: https://doi.org/10.1101/684753

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