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Animal Mitochondrial Genetics

Animal Mitochondrial Genetics

Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...

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Related Experiment Video

Updated: Apr 8, 2026

Understanding the Changes in Mitochondrial Morphology through Dynamic and Three-dimensional Fluorescence Micrographs

Understanding the Changes in Mitochondrial Morphology through Dynamic and Three-dimensional Fluorescence Micrographs

Published on: August 15, 2025

MKK3 deletion improves mitochondrial quality.

Anup Srivastava¹, John McGinniss¹, Yao Wong¹

¹Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520-8057, USA.

Free Radical Biology & Medicine

|June 30, 2015

Summary

This summary is machine-generated.

Mice lacking MAP kinase kinase 3 (MKK3) show improved mitochondrial function and reduced inflammation during sepsis. This suggests MKK3 is a potential therapeutic target for sepsis and other inflammatory diseases.

Keywords:

Cytokines Free radicals Inflammation MKK3 Mitochondria Mitophagy Oxidative phosphorylation

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Published on: August 12, 2018

Area of Science:

Cell Biology
Immunology
Mitochondrial Biology

Background:

Sepsis is a life-threatening condition characterized by excessive inflammation and high mortality in intensive care units.
Mitochondrial dysfunction is implicated in sepsis outcomes.
Previous studies showed MAP kinase kinase 3 (MKK3) knockout mice are resistant to septic injury.

Purpose of the Study:

To investigate the mechanisms underlying improved mitochondrial quality in MKK3 knockout mouse embryonic fibroblasts (MEFs).
To determine the specific role of mitophagy in maintaining mitochondrial health in the absence of MKK3.

Main Methods:

Stimulation of MKK3(-/-) and wild-type (WT) MEFs with lipopolysaccharide (LPS).
Measurement of mitochondrial membrane potential (MMP), ATP levels, cytokine release, and oxidant production.
Transmission electron microscopy (TEM) for mitochondrial morphology assessment.
Stable isotope labeling by/with amino acids in cell culture (SILAC) for proteomic analysis.
Inhibition of mitophagy using Mdivi-1.

Main Results:

MKK3(-/-) MEFs exhibited lower inflammatory cytokine release and oxidant production post-LPS stimulation.
MKK3(-/-) MEFs maintained higher mitochondrial membrane potential (MMP) and ATP levels compared to WT MEFs, even after LPS treatment.
Increased mitophagy and longer, larger mitochondria were observed in MKK3(-/-) MEFs.
Proteomic analysis revealed increased expression of tricarboxylic acid (TCA) cycle enzymes and respiratory complex subunits in MKK3(-/-) MEFs.
Inhibition of mitophagy in MKK3(-/-) MEFs led to decreased MMP and increased cytokine secretion after LPS treatment.

Conclusions:

MKK3 plays a critical role in regulating mitochondrial quality and inflammatory responses.
MKK3 influences mitochondrial protein expression, including TCA cycle enzymes, and mitophagy.
MKK3 deficiency enhances mitochondrial health and confers resistance to inflammatory injury, suggesting MKK3 as a potential therapeutic target for sepsis and inflammatory diseases.