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Related Experiment Video

Updated: Aug 30, 2025

Efficient Differentiation of Mouse Embryonic Stem Cells into Motor Neurons

Efficient Differentiation of Mouse Embryonic Stem Cells into Motor Neurons

Published on: June 9, 2012

KMT5B is required for early motor development.

Jason Hulen¹, Dorothy Kenny¹, Rebecca Black¹

¹Department of Pharmacology and Neuroscience, School of Medicine, Creighton University, Omaha, NE, United States.

Frontiers in Genetics

|August 29, 2022

Summary

This summary is machine-generated.

Lysine methyl transferase 5B (KMT5B) haploinsufficiency in mice impairs motor development, leading to reduced muscle mass and strength. This suggests KMT5B is crucial for skeletal muscle development and neuromuscular function.

Keywords:

H4K20 KMT5B SUV420H histone methylation hypertrophy hypotonia neuromuscular development neuromuscular junction

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Last Updated: Aug 30, 2025

Efficient Differentiation of Mouse Embryonic Stem Cells into Motor Neurons

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Published on: June 9, 2012

A Battery of Motor Tests in a Neonatal Mouse Model of Cerebral Palsy

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Published on: November 3, 2016

Non-Invasive Modulation and Robotic Mapping of Motor Cortex in the Developing Brain

Non-Invasive Modulation and Robotic Mapping of Motor Cortex in the Developing Brain

Published on: July 1, 2019

Area of Science:

Neuroscience
Genetics
Developmental Biology

Background:

Disruptive variants in Lysine Methyltransferase 5B (KMT5B) are linked to human neurodevelopmental disorders, including motor deficits.
The specific role of KMT5B in early motor development remains largely uncharacterized.

Purpose of the Study:

To investigate the function of KMT5B in early motor development using a mouse model.
To assess the impact of KMT5B haploinsufficiency on neuromuscular strength, muscle mass, and skeletal muscle characteristics.

Main Methods:

Utilized a Kmt5b gene trap mouse model.
Assessed neuromuscular strength, skeletal muscle weight, neuromuscular junction (NMJ) structure, and myofiber characteristics at postnatal days 17 and 44.
Examined both slow- and fast-twitch muscle types.

Main Results:

Reduced slow-twitch muscle weight observed in heterozygous males before puberty.
In young adults, KMT5B haploinsufficiency led to decreased neuromuscular strength and skeletal muscle weights in both sexes.
Increased NMJ fragmentation in slow-twitch muscles and smaller myofibers were noted in adult KMT5B-deficient mice.

Conclusions:

KMT5B haploinsufficiency causes significant skeletal muscle developmental deficits.
These deficits manifest as reduced muscle mass, body weight, and impaired neuromuscular function.
KMT5B is essential for normal skeletal muscle development and maintenance.