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Updated: Feb 5, 2026
Measurement of Protein Import Capacity of Skeletal Muscle Mitochondria
Published on: January 7, 2022
Deletion of the microtubule-associated protein 6 (MAP6) results in skeletal muscle dysfunction
Muriel Sébastien1,2, Benoit Giannesini3, Perrine Aubin1,2
1INSERM 1216, Grenoble Institute of Neurosciences, F-38000, Grenoble, France.
Background:
The skeletal muscle fiber has a specific and precise intracellular organization which is at the basis of an efficient muscle contraction. Microtubules are long known to play a major role in the function and organization of many cells, but in skeletal muscle, the contribution of the microtubule cytoskeleton to the efficiency of contraction has only recently been studied. The microtubule network is dynamic and is regulated by many microtubule-associated proteins (MAPs). In the present study, the role of the MAP6 protein in skeletal muscle organization and function has been studied using the MAP6 knockout mouse line.
Methods:
The presence of MAP6 transcripts and proteins was shown in mouse muscle homogenates and primary culture using RT-PCR and western blot. The in vivo evaluation of muscle force of MAP6 knockout (KO) mice was performed on anesthetized animals using electrostimulation coupled to mechanical measurement and multimodal magnetic resonance. The impact of MAP6 deletion on microtubule organization and intracellular structures was studied using immunofluorescent labeling and electron microscopy, and on calcium release for muscle contraction using Fluo-4 calcium imaging on cultured myotubes. Statistical analysis was performed using Student's t test or the Mann-Whitney test.
Results:
We demonstrate the presence of MAP6 transcripts and proteins in skeletal muscle. Deletion of MAP6 results in a large number of muscle modifications: muscle weakness associated with slight muscle atrophy, alterations of microtubule network and sarcoplasmic reticulum organization, and reduction in calcium release.
Conclusion:
Altogether, our results demonstrate that MAP6 is involved in skeletal muscle function. Its deletion results in alterations in skeletal muscle contraction which contribute to the global deleterious phenotype of the MAP6 KO mice. As MAP6 KO mouse line is a model for schizophrenia, our work points to a possible muscle weakness associated to some forms of schizophrenia.
Insights
Microtubule-associated protein 6 (MAP6) is crucial for skeletal muscle function. MAP6 deletion causes muscle weakness, atrophy, and impaired contraction, potentially linking muscle issues to schizophrenia.
Area of Science:
- Cell Biology
- Muscle Physiology
- Neuroscience
Background:
- Skeletal muscle contraction relies on precise intracellular organization.
- Microtubules are vital for cellular function, with their role in skeletal muscle efficiency recently investigated.
- Microtubule-associated proteins (MAPs) regulate the dynamic microtubule network.
Purpose of the Study:
- To investigate the role of MAP6 in skeletal muscle organization and function.
- To analyze the effects of MAP6 deletion on muscle contraction and intracellular structures.
Main Methods:
- Confirmed MAP6 presence in mouse skeletal muscle via RT-PCR and Western blot.
- Assessed in vivo muscle force in MAP6 knockout (KO) mice using electrostimulation and MRI.
- Examined microtubule and sarcoplasmic reticulum organization using immunofluorescence and electron microscopy.
- Measured calcium release in cultured myotubes using Fluo-4 imaging.
Main Results:
- MAP6 transcripts and proteins are present in skeletal muscle.
- MAP6 deletion led to muscle weakness, slight atrophy, altered microtubule and sarcoplasmic reticulum organization, and reduced calcium release.
- MAP6 KO mice exhibited significant muscle modifications.
Conclusions:
- MAP6 plays a significant role in skeletal muscle function.
- MAP6 deletion impairs skeletal muscle contraction, contributing to the phenotype of MAP6 KO mice.
- The findings suggest a potential link between muscle weakness and certain forms of schizophrenia, as modeled by MAP6 KO mice.
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