Detail of Fig4D_WT_MEF
Project
Title
High-magnification electron microimage of mitochondrial structure in control mice MEFs.
Description
High-magnification electron microimage of mitochondrial structure in control mice MEFs.
Release, Updated
2021-09-30
License
CC BY
Kind
Image data
File Formats
.tif
Data size
2.0 MB
Datatype
-
Molecular Function (MF)
-
Biological Process (BP)
gene expression
(
GO:0010467
)
Cellular Component (CC)
mitochondrial crista
(
GO:0030061
)
Biological Imaging Method
electron microscopy
(
Fbbi:00000256
)
X scale
0.014681962 centimeter/pixel
Y scale
0.014681962 centimeter/pixel
Z scale
-
T scale
-
Image Acquisition
Experiment type
-
Microscope type
-
Acquisition mode
-
Contrast method
-
Microscope model
-
Detector model
-
Objective model
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Filter set
-
Summary of Methods
See details in Tanaka H, et. al. (2019) J Cell Sci, 132(11):jcs224766.
Related paper(s)
Hideaki Tanaka, Tomohiko Okazaki, Saeko Aoyama, Mutsumi Yokota, Masato Koike, Yasushi Okada, Yukio Fujiki, Yukiko Gotoh (2019) Peroxisomes control mitochondrial dynamics and the mitochondrion-dependent apoptosis pathway., Journal of cell science, Volume 132, Number 11
Published in 2019 May 31 (Electronic publication in May 31, 2019, midnight )
- doi: 10.1242/jcs.224766
-
pmid: 31076512
(Abstract) Peroxisomes cooperate with mitochondria in the performance of cellular metabolic functions, such as fatty acid oxidation and the maintenance of redox homeostasis. However, whether peroxisomes also regulate mitochondrial fission-fusion dynamics or mitochondrion-dependent apoptosis remained unclear. We now show that genetic ablation of the peroxins Pex3 or Pex5, which are essential for peroxisome biogenesis, results in mitochondrial fragmentation in mouse embryonic fibroblasts (MEFs) in a manner dependent on Drp1 (also known as DNM1L). Conversely, treatment with 4-PBA, which results in peroxisome proliferation, resulted in mitochondrial elongation in wild-type MEFs, but not in Pex3-knockout MEFs. We further found that peroxisome deficiency increased the levels of cytosolic cytochrome c and caspase activity under basal conditions without inducing apoptosis. It also greatly enhanced etoposide-induced caspase activation and apoptosis, which is indicative of an enhanced cellular sensitivity to death signals. Taken together, our data unveil a previously unrecognized role for peroxisomes in the regulation of mitochondrial dynamics and mitochondrion-dependent apoptosis. Effects of peroxin gene mutations on mitochondrion-dependent apoptosis may contribute to pathogenesis of peroxisome biogenesis disorders.This article has an associated First Person interview with the first author of the paper.(MeSH Terms)
- Animals
- Apoptosis/physiology[major]
- Butylamines/pharmacology
- Caspases/metabolism
- Cell Line
- Cytochromes c/metabolism
- Dynamins/metabolism
- Humans
- Lipoproteins/genetics
- Membrane Proteins/genetics
- Mice
- Mice, Inbred C57BL
- Mitochondria/metabolism[major]
- Mitochondrial Dynamics/physiology[major]
- Peroxins/genetics
- Peroxisomal Disorders/pathology
- Peroxisome-Targeting Signal 1 Receptor/genetics
- Peroxisomes/metabolism[major]
- RNA Interference
- RNA, Small Interfering/genetics
Contact
Tomohiko Okazaki
, Hokkaido University
, Institute for Genetic Medicine
, Laboratory of Molecular Cell Biology
Contributors
OMERO Dataset
OMERO Project