Muscle stem cells locally respond to perturbations of motor neurons and the neuromuscular junction.

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.

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.

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.

PTEN mutations disrupt inhibitory GABAergic signaling, causing neurodevelopmental defects that can be mitigated by β-hydroxybutyrate, which activates DAF-16/FOXO and may offer a therapeutic approach for excitation/inhibition imbalances.

A network, composed of 22 relatives of the Beaten Path and Sidestep immunoglobulin superfamily cell surface proteins, also includes several neuronal Beaten Path subfamily receptors which interact selectively with Sidestep subfamily proteins expressed on peripheral tissues.

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.

Fly protein families Dprs and DIPs can create a multitude of complementary interfaces for homo- and heterophilic adhesion complexes, resulting in instructive roles for connectivity in the motor neuron circuitry.