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| Item Type: | Preprint |
|---|---|
| Title: | c-MAF transduces fast motor neuron firing to sustain fast-glycolytic myofibers and neuromuscular junctions |
| Creators Name: | Jauliac, Edgar, Backer, Stephanie, Sadaki, Shunya, Gondin, Julien, Fessard, Aurelie, Escoffier, Hugues, Roullat, Maeva, Di Gallo, Maxime, Levesque, Adrien, Pereira, Doriane, Dos Santos, Mattieu, Vuong, Vincent, Ham, Alexander S., Letourneur, Franck, Pierre, Rémi, Rüegg, Markus A., Birchmeier, Carmen, Fujita, Ryo, Sotiropoulos, Athanassia and Maire, Pascal |
| Abstract: | This study examined how motoneuron activity influences transcription factor binding in mouse fast glycolytic Myh4+ muscle fibers. Single nucleus multiomics of innervated versus denervated tibialis anterior muscles revealed altered chromatin accessibility: SIX and c-MAF binding sites decreased while JUN, FOS, and RUNX1 sites increased in denervated Myh4+ myonuclei. c-MAF showed strong nuclear enrichment after 100 Hz stimulation and periods of increased motoneuron activity but was absent following denervation, establishing it as a primary readout of fast motoneuron firing. Genome-wide analysis demonstrated that c-MAF binding site spacing encodes functionally distinct muscle gene programs. Analysis of constitutive and inducible skeletal muscle-specific c-Maf mutants revealed that c-MAF loss caused region-specific MYH4+ fiber atrophy, MYH1/MYH2 fiber type shifts resembling ALS G93A mouse phenotypes, and progressive neuromuscular junction fragmentation with increased motoneuron terminal sprouting and ectopic reinnervation. These findings establish c-MAF as a critical mediator linking motoneuron activity to muscle gene regulation, fiber integrity, and neuromuscular junction maintenance in fast glycolytic fibers. |
| Keywords: | Animals, Mice |
| Source: | bioRxiv |
| Publisher: | Cold Spring Harbor Laboratory Press |
| Article Number: | 2026.02.05.703983v2 |
| Date: | 17 February 2026 |
| Official Publication: | https://doi.org/10.64898/2026.02.05.703983 |
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