Abstract
Multiple synaptic adhesion molecules govern synapse formation. Here, we propose calsyntenin-3/alcadein-β as a synapse organizer that specifically induces presynaptic differentiation in heterologous synapse-formation assays. Calsyntenin-3 (CST-3) is highly expressed during various postnatal periods of mouse brain development. The simultaneous knockdown of all three CSTs, but not CST-3 alone, decreases inhibitory, but not excitatory, synapse densities in cultured hippocampal neurons. Moreover, the knockdown of CSTs specifically reduces inhibitory synaptic transmission invitro and invivo. Remarkably, the loss of CSTs induces a concomitant decrease in neuron soma size in a non-cell-autonomous manner. Furthermore, α-neurexins (α-Nrxs) are components of a CST-3 complex involved in CST-3-mediated presynaptic differentiation. However, CST-3 does not directly bind to Nrxs. Viewed together, these data suggest that the three CSTs redundantly regulate inhibitory synapse formation, inhibitory synapse function, and neuron development in concert with Nrxs.
| Original language | English |
|---|---|
| Pages (from-to) | 1096-1109 |
| Number of pages | 14 |
| Journal | Cell Reports |
| Volume | 6 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 2014 Mar 27 |
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ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)
Cite this
Calsyntenins Function as Synaptogenic Adhesion Molecules in Concert with Neurexins. / Um, Ji Won; Pramanik, Gopal; Ko, Ji Seung; Song, Min Young; Lee, Dongmin; Kim, Hyun; Park, Kang Sik; Südhof, Thomas C.; Tabuchi, Katsuhiko; Ko, Jaewon.
In: Cell Reports, Vol. 6, No. 6, 27.03.2014, p. 1096-1109.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Calsyntenins Function as Synaptogenic Adhesion Molecules in Concert with Neurexins
AU - Um, Ji Won
AU - Pramanik, Gopal
AU - Ko, Ji Seung
AU - Song, Min Young
AU - Lee, Dongmin
AU - Kim, Hyun
AU - Park, Kang Sik
AU - Südhof, Thomas C.
AU - Tabuchi, Katsuhiko
AU - Ko, Jaewon
PY - 2014/3/27
Y1 - 2014/3/27
N2 - Multiple synaptic adhesion molecules govern synapse formation. Here, we propose calsyntenin-3/alcadein-β as a synapse organizer that specifically induces presynaptic differentiation in heterologous synapse-formation assays. Calsyntenin-3 (CST-3) is highly expressed during various postnatal periods of mouse brain development. The simultaneous knockdown of all three CSTs, but not CST-3 alone, decreases inhibitory, but not excitatory, synapse densities in cultured hippocampal neurons. Moreover, the knockdown of CSTs specifically reduces inhibitory synaptic transmission invitro and invivo. Remarkably, the loss of CSTs induces a concomitant decrease in neuron soma size in a non-cell-autonomous manner. Furthermore, α-neurexins (α-Nrxs) are components of a CST-3 complex involved in CST-3-mediated presynaptic differentiation. However, CST-3 does not directly bind to Nrxs. Viewed together, these data suggest that the three CSTs redundantly regulate inhibitory synapse formation, inhibitory synapse function, and neuron development in concert with Nrxs.
AB - Multiple synaptic adhesion molecules govern synapse formation. Here, we propose calsyntenin-3/alcadein-β as a synapse organizer that specifically induces presynaptic differentiation in heterologous synapse-formation assays. Calsyntenin-3 (CST-3) is highly expressed during various postnatal periods of mouse brain development. The simultaneous knockdown of all three CSTs, but not CST-3 alone, decreases inhibitory, but not excitatory, synapse densities in cultured hippocampal neurons. Moreover, the knockdown of CSTs specifically reduces inhibitory synaptic transmission invitro and invivo. Remarkably, the loss of CSTs induces a concomitant decrease in neuron soma size in a non-cell-autonomous manner. Furthermore, α-neurexins (α-Nrxs) are components of a CST-3 complex involved in CST-3-mediated presynaptic differentiation. However, CST-3 does not directly bind to Nrxs. Viewed together, these data suggest that the three CSTs redundantly regulate inhibitory synapse formation, inhibitory synapse function, and neuron development in concert with Nrxs.
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U2 - 10.1016/j.celrep.2014.02.010
DO - 10.1016/j.celrep.2014.02.010
M3 - Article
VL - 6
SP - 1096
EP - 1109
JO - Cell Reports
JF - Cell Reports
SN - 2211-1247
IS - 6
ER -