Skip to main content
. Author manuscript; available in PMC: 2017 Aug 1.
Published in final edited form as: Curr Opin Cell Biol. 2016 May 26;41:125–131. doi: 10.1016/j.ceb.2016.05.001

Figure 2. The Frizzled Nuclear Import pathway and NE-budding at the Drosophila NMJ.

Figure 2

A high magnification view of the corresponding box in (B) schematically showing the release of Wg via exosomes by presynaptic boutons and the binding of Wg to Fz2 receptors at the ruffled surface of the muscle cell (the subsynaptic reticulum; SSR) is shown (A). The FNI pathway, in which Fz2 receptors are endocytosed at the SSR of the muscle, a cytoplasmic fragment of the receptor (DFz2C) is cleaved, and this fragment is imported into the nucleus (B). A schematic representation of the proposed endogenous NE-budding model, based on EM observations in Drosophila and mouse (C). DFz2C fragments are imported into the nucleus by a mechanism that require nucleoporins and become associated with large RNPs. These RNPs dock at the NE and disrupt the nuclear lamina though a mechanism involving aPKC. Subsequent remodeling of the INM and the ONM, either by pathway 1 (indicated in grey; arrow up) or by pathway 2 (arrow down). The key to the different proteins and structures depicted is shown below panels A–C. MVBs are multivesicular bodies and PSD is the postsynaptic density.