Human skeletal muscle progenitors and motor neurons self-organize in three-dimensional co-culture to form functional neuromuscular junctions that developmentally mature from the embryonic to the adult state.
Proteins implicated in Alzheimer’s disease, including amyloid precursor protein and ApoE receptors, interact with each other and with a signalling molecule called agrin to influence the development of the neuromuscular junction.
Characterization of Tnc as a selective integrin ligand at the Drosophila NMJ allows for unprecedented insights into our understanding of extracellular matrix/integrin interactions at synaptic locations and reveals novel, distinct presynaptic and postsynaptic integrin functions.
Motor axons undergo dynamic branch-specific changes for weeks before complete neuronal degeneration in a model of amyotrophic lateral sclerosis, highlighting the importance of peripheral factors, intrinsic and extrinsic to motoneurons.
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.