{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,2,9]],"date-time":"2026-02-09T23:52:41Z","timestamp":1770681161395,"version":"3.49.0"},"posted":{"date-parts":[[2023,12,22]]},"group-title":"Cell Biology","reference-count":111,"publisher":"openRxiv","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2023,12,22]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                <jats:p>\n                  Adaptor protein complex 4 (AP-4) is a heterotetrameric complex that promotes protein export from the\n                  <jats:italic>trans<\/jats:italic>\n                  -Golgi network. Mutations in each of the AP-4 subunits cause a complicated form of Hereditary Spastic Paraplegia (HSP). Herein, we report that ApoER2, a receptor in the Reelin signaling pathway, is a cargo of the AP-4 complex. We identify the motif ISSF\/Y within the ApoER2 cytosolic domain as necessary for interaction with the canonical signal-binding pocket of the \u00b54 (AP4M1) subunit of AP-4.\n                  <jats:italic>AP4E1<\/jats:italic>\n                  -knock-out (KO) HeLa cells and hippocampal neurons from\n                  <jats:italic>Ap4e1<\/jats:italic>\n                  -KO mice display increased Golgi localization of ApoER2. Furthermore, hippocampal neurons from\n                  <jats:italic>Ap4e1<\/jats:italic>\n                  -KO mice and\n                  <jats:italic>AP4M1<\/jats:italic>\n                  -KO human iPSC-derived cortical i3Neurons exhibit reduced ApoER2 protein expression. Analyses of biosynthetic transport of ApoER2 reveal differential post-Golgi trafficking of the receptor, with lower axonal distribution in KO compared to wild-type neurons, indicating a role of AP-4 and the ISSF\/Y motif in the axonal localization of ApoER2. Finally, analyses of Reelin signaling in mouse hippocampal and human cortical KO neurons show that AP4 deficiency causes no changes in Reelin-dependent activation of the AKT pathway and only mild changes in Reelin-induced dendritic arborization, but reduces Reelin-induced ERK phosphorylation, CREB activation, and Golgi deployment. Altogether, this work establishes ApoER2 as a novel cargo of the AP-4 complex, suggesting that defects in the trafficking of this receptor and in the Reelin signaling pathway could contribute to the pathogenesis of HSP caused by mutations in AP-4 subunits.\n                <\/jats:p>","DOI":"10.1101\/2023.12.21.572896","type":"posted-content","created":{"date-parts":[[2023,12,22]],"date-time":"2023-12-22T14:30:10Z","timestamp":1703255410000},"source":"Crossref","is-referenced-by-count":1,"title":["The Reelin Receptor ApoER2 is a Cargo for the Adaptor Protein Complex AP-4: Implications for Hereditary Spastic Paraplegia"],"prefix":"10.64898","author":[{"given":"Mario 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