The Vesicle‐Mediated Transport Genes, Snap23 , Tmed2 , and Trip10 , are Alternatively Spliced During Striated Muscle Development

The reprogramming of alternative splicing patterns during development is a hallmark tissue maturation and identity. Heart skeletal (striated) muscle tissues exhibit the most highly conserved programs, which substantially change postnatal development. Notably, alterations these events are associated with severe cardiac muscular diseases. In striated muscle, collection genes encoding membrane trafficking proteins spliced in developmental stage-specific manner. However, few splice isoforms have been characterized, little known about their functional roles heart We hypothesize that coordinated represents network, functions to regulate transport cargo critical for homeostasis. Here, we characterize three involved vesicle-mediated alternatively muscle: SNAP23, TMED2, TRIP10. synaptosome-associated protein 23 (SNAP23) SNARE mediates vesicle fusion plasma exocytosis, transmembrane emp23 domain-containing 2 (TMED2) regulates budding secretion, thyroid hormone receptor interactor 10 (TRIP10) endocytosis tubulation. First, found development, Snap23, Tmed2, Trip10 pre-mRNAs undergo changes single exon. Second, transitions characterized by shift from short long isoform expression regulated RBPs quaking (QKI) polypyrimidine tract binding 1 (PTBP1). Third, depletion SNAP23 cells results reduced cell viability differentiation, can be rescued conditioned media differentiated or seeding on collagen-coated plates. Finally, exclusive leads increased myoblasts into myotubes greater myotube area higher nuclei-per-myotube ratio. Taken together, our data suggest Snap23 an important regulator myogenesis, where controls secretion necessary size. Preliminary studies show disruption TMED2 TRIP10 levels likewise affects differentiation. Elucidating mechanisms regulation consequences networks will fundamental understanding disease.