BMPR-2 gates activity-dependent stabilization of primary dendrites during mitral cell remodeling

Shuhei Aihara, Satoshi Fujimoto, Richi Sakaguchi, Takeshi Imai

研究成果: Contribution to journalArticle査読

抄録

Developing neurons initially form excessive neurites and then remodel them based on molecular cues and neuronal activity. Developing mitral cells in the olfactory bulb initially extend multiple primary dendrites. They then stabilize single primary dendrites while eliminating others. However, the mechanisms underlying selective dendrite remodeling remain elusive. Using CRISPR-Cas9-based knockout screening combined with in utero electroporation, we identify BMPR-2 as a key regulator for selective dendrite stabilization. Bmpr2 knockout and its rescue experiments show that BMPR-2 inhibits LIMK without ligands and thereby permits dendrite destabilization. In contrast, the overexpression of antagonists and agonists indicates that ligand-bound BMPR-2 stabilizes dendrites, most likely by releasing LIMK. Using genetic and FRET imaging experiments, we demonstrate that free LIMK is activated by NMDARs via Rac1, facilitating dendrite stabilization through F-actin formation. Thus, the selective stabilization of primary dendrites is ensured by concomitant inputs of BMP ligands and neuronal activity.

本文言語英語
論文番号109276
ジャーナルCell Reports
35
12
DOI
出版ステータス出版済み - 6 22 2021

All Science Journal Classification (ASJC) codes

  • 生化学、遺伝学、分子生物学(全般)

フィンガープリント

「BMPR-2 gates activity-dependent stabilization of primary dendrites during mitral cell remodeling」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル