Figure S1. No differences in body weight, gross cerebellar architecture, and motorcoordination between wild-type and GluK4 KO mice, Related to Figures 1 and 2. -- Figure S2. Basic CF- and PF-EPSC properties in wild-type and GluK4 KO mice, Related to Figure 1. -- Figure S3. The KAR components are absent in CF-EPSCs of GluK1 KO and GluK4 KO mice, and CF-EPSCs are reduced in PC-specific GluK4 KO mice, Related to Figure 1. -- Figure S4. The GluK1 KO cerebellum exhibited a reduction in CFPC synapses, Related to Figure 3. -- Figure S5. PF/ΔV-stim failed to induce LTD in C1ql1 KO and Bai3 KO PCs, Related to Figure 2. -- Figure S6. Mono CF innervation to single PC in adult GluK4 KO mice. -- Figure S7. MAP allows immunodetection of endogenous GluK4 at CFPC synapse. -- Figure S8. GluK4 and C1ql1 signals on vGluT2-positive area in GluK4 KO, C1ql1 KO and Bai3 KO mice. -- Figure S9. C1ql1 binds to the ATD of GluK4 but not GluK1 in vitro. -- Figure S10. The ATD of GluK4 indirectly binds to Bai3 via C1ql1 in vitro. -- Figure S11. KAR-mediated currents in GluK4 KO PCs expressing HA-GluK4. -- Figure S12. No KAR component at PF-EPSCs in GluK4 KO PCs overexpressing GluK4. -- Figure S13. Transduction efficiency of PCs by retro-orbital injection of AAV(PHP.eB. -- Figure S14. A proposed model illustrating the KAR−C1ql1−Bai3 complex on CF−PC synapses for synaptic integrity, LTD and motor learning

Peer reviewed