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. 2020 Aug 2;15:11. doi: 10.1186/s13064-020-00147-5

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — BMP Canonical and Non-Canonical signaling at the NMJ. a BMP canonical signaling includes a paracrine, retrograde mechanism whereby muscle-derived Gbb is released across the synapse where it activates BMPRs Wit and Sax/Tkv triggering internalization. Internalized Gbb is trafficked to the neuronal nucleus where it activates phosphorylation of the Mad to pMad to activate transcription of Trio-GEF promoting overall NMJ growth. A second autocrine canonical pathway involves release of Cmpy bound Gbb from the neuron where it sequestered by α₂δ-3, a calcium channel subunit. Neuronally derived Gbb then binds BMPRs and causes transcriptional changes similar to the paracrine canonical pathway to regulate synaptic homeostasis and signal transmission. b BMP non-canonical signaling pathways include those that are Gbb dependent and independent. Gbb dependent non-canonical signaling involves retrograde release of Gbb where it is bound by Wit. LIMK acts as a Wit effector to inhibit Cofilin which normally promotes actin dynamics through filament severing. In a Gbb independent non-canonical mechanism, GluRIIA containing iGluRs form a positive feedback loop with local presynaptic pMad. This mechanism depends on Wit and Sax/Tkv, but not on transcription and is inhibited by Dlp (Glypican)