論文

査読有り
2009年1月

Ca2+ induces macropinocytosis via F-actin depolymerization during growth cone collapse

MOLECULAR AND CELLULAR NEUROSCIENCE
  • Hiroyuki Kabayama
  • ,
  • Takeshi Nakamura
  • ,
  • Makoto Takeuchi
  • ,
  • Hirohide Iwasaki
  • ,
  • Masahiko Taniguchi
  • ,
  • Naoko Tokushige
  • ,
  • Katsuhiko Mikoshiba

40
1
開始ページ
27
終了ページ
38
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.mcn.2008.08.009
出版者・発行元
ACADEMIC PRESS INC ELSEVIER SCIENCE

Growth cone collapse occurs in repulsive axon guidance and is accompanied by a reduction in the surface area of the plasma membrane of growth cones. However, the mechanism of this reduction is unclear. Here, we show that during growth cone collapse, caffeine-induced Ca2+ release from ryanodine-sensitive Ca2+ Stores triggers the formation of large vacuoles in growth cones by macropinocytosis, a clathrin-independent endocytosis for the massive retrieval of the cellular plasma membrane, and Subsequent retrograde membrane transport. We observed a significant correlation of the area of caffeine-induced macropinosomes with growth cone collapse. We also detected macropinocytosis induced by semaphorin 3A, a typical repulsive cue, and correlation between the area of semaphorin 3A-induced macropinocytic vacuoles and growth cone collapse. Moreover, jasplakinolide, an inhibitor of F-actin depolymerization, blocked caffeine-induced macropinocytosis. We propose that the coordinated regulation of actin cytoskeletal reorganization and macropinocytosis-mediated retrograde membrane trafficking may contribute to Ca2+-induced axon growth inhibition. (C) 2008 Elsevier Inc. All rights reserved.

リンク情報
DOI
https://doi.org/10.1016/j.mcn.2008.08.009
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/18848894
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000262422700003&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.mcn.2008.08.009
  • ISSN : 1044-7431
  • PubMed ID : 18848894
  • Web of Science ID : WOS:000262422700003

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