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Innervation of the masseter requires Mllt11 (Af1q/Tcf7c) function during trigeminal ganglion development
Nicholas W Zinck1, Danielle Stanton-Turcotte1, Emily A Witt1
1Department of Medical Neuroscience, and Brain Repair Centre, Faculty of Medicine, Dalhousie University, Life Science Research Institute, Halifax, Nova Scotia, Canada.
The International Journal of Developmental Biology
|August 1, 2025
Summary
The study reveals Mllt11 is crucial for trigeminal nerve development and masseter muscle innervation. Loss of Mllt11 alters cellular composition of the trigeminal ganglion and impairs motor function.
Area of Science:
- Neuroscience
- Developmental Biology
- Molecular Biology
Background:
- Cranial nerve development and neuromuscular junction (NMJ) formation are vital for craniofacial motor function.
- Mllt11 (also known as Af1q/Tcf7c) is a cytoskeletal protein involved in central nervous system development, but its peripheral roles are unclear.
Purpose of the Study:
- To investigate the function of Mllt11 in trigeminal nerve development and its impact on masseter muscle innervation.
- To understand Mllt11's role in the cellular composition of the trigeminal ganglion.
Main Methods:
- Utilized a conditional knockout mouse model to delete Mllt11 in Wnt1-expressing neural crest cells.
- Assessed trigeminal ganglion development, cellular composition, and masseter muscle innervation.
- Analyzed neurofilament density, NMJ formation, and branchiomotor neuron populations.
Main Results:
- Mllt11 expression was detected in developing trigeminal ganglia.
- Mllt11 loss did not affect initial trigeminal ganglion formation but altered its placodal vs. neural crest cellular composition.
- Conditional Mllt11 inactivation reduced neurofilament density and NMJs in the masseter muscle, with reduced Phox2b+ branchiomotor neurons, indicating impaired trigeminal motor innervation.
Conclusions:
- Mllt11 regulates the cellular composition of the trigeminal ganglion.
- Mllt11 is essential for proper trigeminal motor innervation of the masseter muscle.
- The Wnt1Cre2 driver showed unexpected recombination in branchiomotor neurons, impacting results.
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