Required for the maintenance of appropriate synaptic retrograde communication and the stabilization of muscle cell architecture or physiology. Both det and Dg are required for maintenance of early dpp signaling in the presumptive crossvein. Isoform A is not required to maintain muscle integrity, but plays a role in neuromuscular homeostasis by regulating neurotransmitter release. May play a role in anchoring the cytoskeleton to the plasma membrane. Component of the dystrophin associated protein complex (DAPC). Interacts with Dg, via the Dg WW domain binding sites. Isoform A is localized to both the postsynaptic region of the NMJ and to the extrasynaptic regions, where it colocalizes with actin. Isoform A, isoform F and isoform G are expressed in the midgut endoderm of stage 12 embryos. In stage 16 embryos, expression is also seen in the pericardial cells, cells at the ectoderm segmental border and cells along the midline of the CNS. During embryogenesis, isoform A is also expressed in the visceral mesoderm, muscle attachment sites, mesectodermal cells at the midline, the gut, and throughout muscle fibers. In larvae, isoform A is found in all muscle fibers, but not detectable in the brain or neuropil. Isoform A is expressed in embryos and larvae and levels increase further in adults. Isoform F has weak expression in embryos, increases in larvae and falls again in adults. Isoform G is weakly expressed in adult flies, and not detectable earlier in development. Wings exhibit a 'crossveinless' phenotype. Adult flies are viable and the crossvein defect is the sole overt morphological defect observed. Flies that have reduced expression of all isoforms (due to transgenic RNA interference targeting the common C-terminal region) exhibit severe muscle degeneration in larvae and adult flies. Muscles were either ruptured, absent or the fibers were detached from their attachment sites at tendon cells. These are necrotic, not apoptotic processes.