The RhoGAP crossveinless-c interacts with Dystrophin and is required for synaptic homeostasis at the Drosophila neuromuscular junction.

ABSTRACT: Duchenne muscular dystrophy is caused by mutations in the Dystrophin gene and is characterized by muscle degeneration and the occurrence of mental deficits in a significant number of patients. Although Dystrophin and its closely related ortholog Utrophin are present at a variety of synapses, little is known about their roles in the nervous system. Previously, we reported that absence of postsynaptic Dystrophin from the Drosophila neuromuscular junction (NMJ) disrupts synaptic homeostasis, resulting in increased stimulus-evoked neurotransmitter release. Here, we show that RhoGAP crossveinless-c (cv-c), a negative regulator of Rho GTPase signaling pathways, genetically interacts with Dystrophin. Electrophysiological characterization of the cv-c-deficient NMJ and the use of presynaptic- and p

SUBMITTER: Pilgram GS 

PROVIDER: S-EPMC6623439 | biostudies-literature | 2011 Jan

REPOSITORIES: biostudies-literature