Dystrophin is required for appropriate retrograde control of neurotransmitter release at the Drosophila neuromuscular junction.

ABSTRACT: Mutations in the human dystrophin gene cause the Duchenne and Becker muscular dystrophies. The Dystrophin protein provides a structural link between the muscle cytoskeleton and extracellular matrix to maintain muscle integrity. Recently, Dystrophin has also been found to act as a scaffold for several signaling molecules, but the roles of dystrophin-mediated signaling pathways remain unknown. To further our understanding of this aspect of the function of dystrophin, we have generated Drosophila mutants that lack the large dystrophin isoforms and analyzed their role in synapse function at the neuromuscular junction. In expression and rescue studies, we show that lack of the large dystrophin isoforms in the postsynaptic muscle cell leads to elevated evoked neurotransmitter release from the pr

SUBMITTER: van der Plas MC 

PROVIDER: S-EPMC6674336 | biostudies-literature | 2006 Jan

REPOSITORIES: biostudies-literature