7CEE
Crystal structure of mouse neuroligin-3
Summary for 7CEE
| Entry DOI | 10.2210/pdb7cee/pdb |
| Descriptor | Neuroligin-3, 2-acetamido-2-deoxy-beta-D-glucopyranose (3 entities in total) |
| Functional Keywords | synapse organization, trans-synaptic complex, esterase domain, cell adhesion |
| Biological source | Mus musculus (Mouse) |
| Total number of polymer chains | 2 |
| Total formula weight | 146869.88 |
| Authors | Yamagata, A.,Yoshida, T.,Shiroshima, T.,Maeda, A.,Fukai, S. (deposition date: 2020-06-23, release date: 2021-02-24, Last modification date: 2024-11-06) |
| Primary citation | Yoshida, T.,Yamagata, A.,Imai, A.,Kim, J.,Izumi, H.,Nakashima, S.,Shiroshima, T.,Maeda, A.,Iwasawa-Okamoto, S.,Azechi, K.,Osaka, F.,Saitoh, T.,Maenaka, K.,Shimada, T.,Fukata, Y.,Fukata, M.,Matsumoto, J.,Nishijo, H.,Takao, K.,Tanaka, S.,Okabe, S.,Tabuchi, K.,Uemura, T.,Mishina, M.,Mori, H.,Fukai, S. Canonical versus non-canonical transsynaptic signaling of neuroligin 3 tunes development of sociality in mice. Nat Commun, 12:1848-1848, 2021 Cited by PubMed Abstract: Neuroligin 3 (NLGN3) and neurexins (NRXNs) constitute a canonical transsynaptic cell-adhesion pair, which has been implicated in autism. In autism spectrum disorder (ASD) development of sociality can be impaired. However, the molecular mechanism underlying NLGN3-mediated social development is unclear. Here, we identify non-canonical interactions between NLGN3 and protein tyrosine phosphatase δ (PTPδ) splice variants, competing with NRXN binding. NLGN3-PTPδ complex structure revealed a splicing-dependent interaction mode and competition mechanism between PTPδ and NRXNs. Mice carrying a NLGN3 mutation that selectively impairs NLGN3-NRXN interaction show increased sociability, whereas mice where the NLGN3-PTPδ interaction is impaired exhibit impaired social behavior and enhanced motor learning, with imbalance in excitatory/inhibitory synaptic protein expressions, as reported in the Nlgn3 R451C autism model. At neuronal level, the autism-related Nlgn3 R451C mutation causes selective impairment in the non-canonical pathway. Our findings suggest that canonical and non-canonical NLGN3 pathways compete and regulate the development of sociality. PubMed: 33758193DOI: 10.1038/s41467-021-22059-6 PDB entries with the same primary citation |
| Experimental method | X-RAY DIFFRACTION (2.763 Å) |
Structure validation
Download full validation report
