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タイトル: | Discovery of long-range inhibitory signaling to ensure single axon formation |
著者: | Takano, Tetsuya Wu, Mengya Nakamuta, Shinichi Naoki, Honda https://orcid.org/0000-0001-6816-9126 (unconfirmed) Ishizawa, Naruki Namba, Takashi Watanabe, Takashi Xu, Chundi Hamaguchi, Tomonari Yura, Yoshimitsu Amano, Mutsuki Hahn, Klaus M. Kaibuchi, Kozo |
著者名の別形: | 本田, 直樹 |
キーワード: | Cellular neuroscience Neuronal development |
発行日: | 26-Jun-2017 |
出版者: | Springer Nature |
誌名: | Nature Communications |
巻: | 8 |
論文番号: | 33 |
抄録: | A long-standing question in neurodevelopment is how neurons develop a single axon and multiple dendrites from common immature neurites. Long-range inhibitory signaling from the growing axon is hypothesized to prevent outgrowth of other immature neurites and to differentiate them into dendrites, but the existence and nature of this inhibitory signaling remains unknown. Here, we demonstrate that axonal growth triggered by neurotrophin-3 remotely inhibits neurite outgrowth through long-range Ca[2+] waves, which are delivered from the growing axon to the cell body. These Ca[2+] waves increase RhoA activity in the cell body through calcium/calmodulin-dependent protein kinase I. Optogenetic control of Rho-kinase combined with computational modeling reveals that active Rho-kinase diffuses to growing other immature neurites and inhibits their outgrowth. Mechanistically, calmodulin-dependent protein kinase I phosphorylates a RhoA-specific GEF, GEF-H1, whose phosphorylation enhances its GEF activity. Thus, our results reveal that long-range inhibitory signaling mediated by Ca[2+] wave is responsible for neuronal polarization. |
著作権等: | © The Author(s) 2017. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. |
URI: | http://hdl.handle.net/2433/226512 |
DOI(出版社版): | 10.1038/s41467-017-00044-2 |
PubMed ID: | 28652571 |
出現コレクション: | 学術雑誌掲載論文等 |
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