Springer Berlin Heidelberg
Berlin/Heidelberg
Springer
424
10.1007/424.1432-2013
0031-6768
1432-2013
Pflügers Archiv - European Journal of Physiology
European Journal of Physiology
Pflugers Arch - Eur J Physiol
Biomedicine
Human Physiology
Molecular Medicine
Neurosciences
Cell Biology
Receptors
Biomedical and Life Sciences
470
470
12
8
8
Special Focus on: Mitochondrial Signalling
11
2018
7
13
2018
7
13
2018
8
2018
Springer-Verlag GmbH Germany, part of Springer Nature
2018
Ole
Petersen
Alexei
Tepikin
2133
10.1007/s00424-018-2133-0
6
Intracellular Ca2+ release decelerates mitochondrial cristae dynamics within the junctions to the endoplasmic reticulum
Original Article
1193
1203
2018
2
27
2017
12
13
2018
2
24
2018
2
26
2018
3
12
Austrian Science Fund
W 1226-B18
BioTechMed Graz
The Author(s)
2018
Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
Benjamin
Gottschalk
Christinae
Klec
Markus
Waldeck-Weiermair
Roland
Malli
Wolfgang
F.
Graier
+43 316 385 71963
wolfgang.graier@medunigraz.at
0000 0000 8988 2476
grid.11598.34
Molecular Biology and Biochemistry, Gottfried Schatz Research Center
Medical University of Graz
Neue Stiftingtalstraße 6/6
8010
Graz
Austria
grid.452216.6
BioTechMed
Graz
Austria
Abstract
Mitochondria are multifunctional organelles that essentially contribute to cell signaling by sophisticated mechanisms of communications. Live cell imaging studies showed that mitochondria are dynamic and complex structures that form ramified networks by directed movements, fission, and fusion events. There is emerging evidence that the morphology of mitochondria determines cellular functions and vice versa. Several intracellular signaling pathways and messengers including Ca2+ dynamically influence the architecture of mitochondria. Because electron microscopy cannot be utilized for an assessment of dynamics of mitochondrial morphology in intact cells, most studies were performed using wide-field or laser confocal fluorescence microscopies that, due to limitations of their spatial resolution, do not allow investigating sub-mitochondrial structures. Accordingly, our understanding of the dynamics of substructures of mitochondria is quite limited. Here, we present a robust super-resolution method to quantify the dynamics of mitochondrial cristae, the main substructures of the inner mitochondrial membrane, exploiting structured illumination microscopy (SIM). We observed that knockdown of the dynamin-like 120-kDa protein, which is encoded by the OPA1 gene, specifically reduces the dynamics of the mitochondrial cristae membranes (CM), while the inner boundary membrane (IBM) remained flexible. We further used dual color SIM to quantify the dynamics of CM in the junction between mitochondria and the endoplasmic reticulum (ER; mitochondrial associated membranes, MAMs). Intracellular Ca2+ release spatially reduced CM-dynamics in MAMs. Moreover, CM-dynamics was independent from matrix Ca2+ signal. Our data suggest that local Ca2+ signals specifically control CM-dynamics and structure to facilitate a well-balanced functional (Ca2+) interplay between mitochondria and the ER.
Keywords
Cristae dynamics
Microscopy
Mitochondria
Mitochondrial Ca2+
Mitochondria-associated membranes
OPA1
MCU
Structured illumination microscopy
This article is part of the special issue on Mitochondrial Signalling in Pflügers Archiv – European Journal of Physiology
Electronic supplementary material
The online version of this article (https://doi.org/10.1007/s00424-018-2133-0) contains supplementary material, which is available to authorized users.
ftp_PUB_18-07-14_05-09-39.zip424-2018-Article-2133.pdfPDF1.4