Fig. 8: Working model of synaptopathology in a Drosophila larval NMJ model of DM1. | Nature Communications

Fig. 8: Working model of synaptopathology in a Drosophila larval NMJ model of DM1.

From: Pre- and postsynaptic upregulation of FasII synergistically underlies neuropathological and behavioral phenotypes in a Drosophila model of myotonic dystrophy

Fig. 8

a Under the normal condition, FasII-A-PEST+ and FasII-A-PEST− are the major isoforms present at the pre- and postsynaptic terminals. Both FasII-A isoforms convey intracellular signals to maintain synapse integrity. Postsynaptic FasII-A are capable of interacting with DLG, and may facilitate retrograde signals that help with maintaining bouton numbers. b Under the DM1-like condition, expanded CUG repeats causes upregulation of overall FasII, which in turn causes an abnormally high level of FasII-C at the synapse. FasII-C may bind to itself or compete with other isoforms to bind to the FasII-A isoforms. Since the FasII-C isoform lacks the cytoplasmic domain, its binding to FasII-A disrupts the intracellular signals required for maintaining synapse integrity.

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