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. Author manuscript; available in PMC: 2023 Jan 19.
Published in final edited form as: Neuron. 2021 Nov 29;110(2):195–208. doi: 10.1016/j.neuron.2021.10.035

Figure 3:

Figure 3:

Alternative splicing of Syngap1 gives rise to SynGAP isoforms with distinct, temporally-regulated subcellullar localization in immature and mature neurons. Earlier and less synaptically-enriched expression of the β isoform of SynGAP in immature neurons (left) results in a specific role for this classical synaptic protein in dendritic arborization. In mature neurons (right), SynGAP-α1 is enriched at the postsynaptic density, where it directly interacts with PSD-95 and regulates synaptic plasticity. Dendritic arborization is altered in human neurons lacking all SYNGAP1 isoforms, but it is not yet clear in human cells how this developmental reorganization of SynGAP isoforms might be influenced by SYNGAP1 mutations.