Morphology and FRET/Ca2+ imaging data of mitral cells in the mouse olfactory bulb.
See detail in Aihara S, Fujimoto S, Sakaguchi R, Imai T. BMPR-2 gates activity-dependent stabilization of primary dendrites during mitral cell remodeling. Cell Rep. 2021 Jun 22;35(12):109276. doi: 10.1016/j.celrep.2021.109276. PMID: 34161760.
Shuhei Aihara, Satoshi Fujimoto, Richi Sakaguchi, Takeshi Imai (2021) BMPR-2 gates activity-dependent stabilization of primary dendrites during mitral cell remodeling., Cell reports, Volume 35, Number 12, pp. 109276
Published in 2021 Jun 22
(Abstract) 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.(MeSH Terms)
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