Skeletal muscle stem cells play important roles in the regeneration of neuromuscular junctions, and so present new targets for therapies to treat neuromuscular decline observed in the context of aging and various neuromuscular diseases.
Building on previous work (Liu et al., 2015), it is shown that depletion or rescue of adult skeletal muscle stem cells is sufficient to induce or attenuate age-associated neuromuscular junction deterioration respectively.
Neurexin–Neuroligin1 complex positively regulates F-actin assembly through direct interaction with WAVE complex to control normal synaptic growth and electrophysiological function in Drosophila neuromuscular junction.
Maintenance of peripheral myonuclei patterning in skeletal myofibers is dependent on the regulation of microtubules dynamic and nuclei motion and is essential for proper neuromuscular junction integrity and mitochondria homeostasis.
In vivo stem cell reprogramming in the well-studied stem cell NB7-1 using the classic temporal transcription factor Hunchback increases motor neuron number and re-specifies dendritic morphology and neuromuscular synaptic partnerships.