Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

19.8K
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
19.8K
Energy to Drive Translocation01:37

Energy to Drive Translocation

3.0K
Mitochondrial protein import is powered by two distinct energy sources: ATP hydrolysis and electrochemical potential across the inner membrane. Newly synthesized precursors are bound by cytosolic chaperones of the Hsp70 family, which guide them to the import receptors on the mitochondrial surface. Utilizing the energy of ATP hydrolysis, Hsp70 chaperones transfer these precursors to the TOM receptors on the mitochondrial outer membrane.
Generally, polypeptides are unfolded by two distinct...
3.0K
Necrosis01:16

Necrosis

7.4K
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
7.4K
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

13.8K
Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
13.8K
ATP Synthase: Mechanism01:48

ATP Synthase: Mechanism

19.1K
In animals, the mitochondrial F1F0 ATP synthase is the key protein that synthesizes ATP molecules through a complex catalytic mechanism. While the nuclear genome encodes the majority of ATP synthase subunits, the mitochondrial genome encodes some of the enzyme's most critical components. The formation of this multi-subunit enzyme is a complex multi-step process regulated at the level of transcription, translation, and assembly. Defects in one or more of these steps can result in decreased...
19.1K
The Electron Transport Chain01:30

The Electron Transport Chain

21.8K
The electron transport chain or oxidative phosphorylation is an exothermic process in which free energy released during electron transfer reactions is coupled to ATP synthesis. This process is a significant source of energy in aerobic cells, and therefore inhibitors of the electron transport chain can be detrimental to the cell's metabolic processes.
Inhibitors of the electron transport chain
Rotenone, a widely used pesticide, prevents electron transfer from Fe-S cluster to ubiquinone or Q...
21.8K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Grapefruit By-Products as a Sustainable Source of Bioaccessible Polyphenols with In Vitro Neuroprotective Potential.

International journal of molecular sciences·2026
Same author

An innovative in vitro model for studying the biology of cardiac fibroblasts originating from the epicardium.

Disease models & mechanisms·2026
Same author

Exploration of the mutational landscape of cutaneous leiomyoma confirms FH as a driver gene and identifies targeting purine metabolism as a potential therapeutic strategy.

The British journal of dermatology·2024
Same author

Endothelial TDP-43 controls sprouting angiogenesis and vascular barrier integrity, and its deletion triggers neuroinflammation.

JCI insight·2024
Same author

FOXA2 controls the anti-oxidant response in FH-deficient cells.

Cell reports·2023
Same author

G9a Inhibition Promotes Neuroprotection through GMFB Regulation in Alzheimer's Disease.

Aging and disease·2023

Related Experiment Video

Updated: Apr 16, 2026

Assessment of Mitochondrial Fission/Fusion Dynamics in Kidney Proximal Tubular Cells
06:14

Assessment of Mitochondrial Fission/Fusion Dynamics in Kidney Proximal Tubular Cells

Published on: November 14, 2025

790

Mitochondrial fragmentation in excitotoxicity requires ROCK activation.

Alejandro Martorell-Riera1, Marc Segarra-Mondejar, Manuel Reina

  • 1a Department of Cell Biology and CELLTEC-UB; Faculty of Biology ; University of Barcelona ; Barcelona , Spain.

Cell Cycle (Georgetown, Tex.)
|March 20, 2015
PubMed
Summary
This summary is machine-generated.

Mitochondrial fission, crucial for cell death, involves dynamin-related protein 1 (Drp1) and the actomyosin system. ROCK activation, not directly on Drp1, regulates this process during excitotoxicity, offering new therapeutic targets.

Keywords:
Drp1actomyosinexcitotoxicitymitocondrial dynamicsneuron

More Related Videos

A Faster, High Resolution, mtPA-GFP-based Mitochondrial Fusion Assay Acquiring Kinetic Data of Multiple Cells in Parallel Using Confocal Microscopy
10:45

A Faster, High Resolution, mtPA-GFP-based Mitochondrial Fusion Assay Acquiring Kinetic Data of Multiple Cells in Parallel Using Confocal Microscopy

Published on: July 20, 2012

17.3K
Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess
07:35

Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess

Published on: June 1, 2022

2.7K

Related Experiment Videos

Last Updated: Apr 16, 2026

Assessment of Mitochondrial Fission/Fusion Dynamics in Kidney Proximal Tubular Cells
06:14

Assessment of Mitochondrial Fission/Fusion Dynamics in Kidney Proximal Tubular Cells

Published on: November 14, 2025

790
A Faster, High Resolution, mtPA-GFP-based Mitochondrial Fusion Assay Acquiring Kinetic Data of Multiple Cells in Parallel Using Confocal Microscopy
10:45

A Faster, High Resolution, mtPA-GFP-based Mitochondrial Fusion Assay Acquiring Kinetic Data of Multiple Cells in Parallel Using Confocal Microscopy

Published on: July 20, 2012

17.3K
Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess
07:35

Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess

Published on: June 1, 2022

2.7K

Area of Science:

  • Cell Biology
  • Neuroscience
  • Mitochondrial Dynamics

Background:

  • Mitochondrial morphology, regulated by fission and fusion, is vital for cellular homeostasis.
  • Mitochondrial fission is implicated in cell death pathways, particularly during excitotoxic insults.
  • Dynamin-related protein 1 (Drp1) is a key mediator of mitochondrial fission, activated through post-translational modifications like nitrosylation.

Purpose of the Study:

  • To investigate the role of the actomyosin system and ROCK in excitotoxicity-induced mitochondrial fragmentation.
  • To elucidate the relationship between ROCK, Drp1, and mitochondrial fission under excitotoxic conditions.

Main Methods:

  • Utilized primary cortical neurons subjected to excitotoxic insults.
  • Employed phosphor-mutant forms of Drp1 to differentiate direct and indirect ROCK actions.
  • Assessed mitochondrial fragmentation and the involvement of nitric oxide and ROCK signaling.

Main Results:

  • Excitotoxicity-induced mitochondrial fragmentation requires both nitric oxide production and ROCK activation.
  • ROCK does not directly phosphorylate Drp1 to mediate fission in excitotoxic conditions.
  • ROCK likely acts on the actomyosin complex, which is essential for mitochondrial fission.

Conclusions:

  • Mitochondrial fragmentation during excitotoxicity involves a complex interplay between Drp1, nitric oxide, and the ROCK-activated actomyosin system.
  • ROCK's role in fission appears indirect, targeting the actomyosin machinery rather than Drp1 directly.
  • Targeting pathways beyond Drp1, including the actomyosin system, presents a promising therapeutic strategy to prevent mitochondrial fragmentation.