論文 - 詳細
| RRC ID | 77500 |
|---|---|
| 著者 | Kastian RF, Minegishi T, Baba K, Saneyoshi T, Katsuno-Kambe H, Saranpal S, Hayashi Y, Inagaki N. |
| タイトル | Shootin1a-mediated actin-adhesion coupling generates force to trigger structural plasticity of dendritic spines. |
| ジャーナル | Cell Rep |
| Abstract |
Dendritic spines constitute the major compartments of excitatory post-synapses. They undergo activity-dependent enlargement, which is thought to increase the synaptic efficacy underlying learning and memory. The activity-dependent spine enlargement requires activation of signaling pathways leading to promotion of actin polymerization within the spines. However, the molecular machinery that suffices for that structural plasticity remains unclear. Here, we demonstrate that shootin1a links polymerizing actin filaments in spines with the cell-adhesion molecules N-cadherin and L1-CAM, thereby mechanically coupling the filaments to the extracellular environment. Synaptic activation enhances shootin1a-mediated actin-adhesion coupling in spines. Promotion of actin polymerization is insufficient for the plasticity; the enhanced actin-adhesion coupling is required for polymerizing actin filaments to push against the membrane for spine enlargement. By integrating cell signaling, cell adhesion, and force generation into the current model of actin-based machinery, we propose molecular machinery that is sufficient to trigger the activity-dependent spine structural plasticity. |
| 巻・号 | 35(7) |
| ページ | 109130 |
| 公開日 | 2021-5-18 |
| DOI | 10.1016/j.celrep.2021.109130 |
| PII | S2211-1247(21)00469-1 |
| PMID | 34010643 |
| MeSH | Actins / metabolism Animals Dendritic Spines / metabolism Humans Mice Nerve Tissue Proteins / metabolism* Neuronal Plasticity |
| IF | 8.109 |
| オルトメトリクス指標 |
オルトメトリクス指標項目
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| 最多言及媒体 | X(Twitter) |
| 各媒体での言及数の合計 | 11 |
| 過去6か月間でのオルトメトリクス指標の変動値 | 0.0 |
| リソース情報 | |
| 遺伝子材料 | pCAGGS-myc-shootin1a (30-146) (RDB19945) |