| First Author | Ban Y | Year | 2021 |
| Journal | Sci Adv | Volume | 7 |
| Issue | 41 | Pages | eabh2974 |
| PubMed ID | 34613779 | Mgi Jnum | J:346427 |
| Mgi Id | MGI:6787980 | Doi | 10.1126/sciadv.abh2974 |
| Citation | Ban Y, et al. (2021) Prickle promotes the formation and maintenance of glutamatergic synapses by stabilizing the intercellular planar cell polarity complex. Sci Adv 7(41):eabh2974 |
| abstractText | Whether there exists a common signaling mechanism that assembles all glutamatergic synapses is unknown. We show here that knocking out Prickle1 and Prickle2 reduced the formation of the PSD-95âpositive glutamatergic synapses in the hippocampus and medial prefrontal cortex in postnatal development by 70â80%. Prickle1 and Prickle2 double knockout in adulthood lead to the disassembly of 70 to 80% of the postsynaptic-density(PSD)-95âpositive glutamatergic synapses. PSD-95âpositive glutamatergic synapses in the hippocampus of Prickle2E8Q/E8Q mice were reduced by 50% at postnatal day 14. Prickle2 promotes synapse formation by antagonizing Vangl2 and stabilizing the intercellular complex of the planar cell polarity (PCP) components, whereas Prickle2 E8Q fails to do so. Coculture experiments show that the asymmetric PCP complexes can determine the presynaptic and postsynaptic polarity. In summary, the PCP components regulate the assembly and maintenance of a large number of glutamatergic synapses and specify the direction of synaptic transmission. |
