論文

査読有り
2017年4月

Distinct intracellular Ca2+ dynamics regulate apical constriction and differentially contribute to neural tube closure

DEVELOPMENT
  • Makoto Suzuki
  • Masanao Sato
  • Hiroshi Koyama
  • Yusuke Hara
  • Kentaro Hayashi
  • Naoko Yasue
  • Hiromi Imamura
  • Toshihiko Fujimori
  • Takeharu Nagai
  • Robert E. Campbell
  • Naoto Ueno
  • 全て表示

144
7
開始ページ
1307
終了ページ
1316
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1242/dev.141952
出版者・発行元
COMPANY OF BIOLOGISTS LTD

Early in the development of the central nervous system, progenitor cells undergo a shape change, called apical constriction, that triggers the neural plate to form a tubular structure. How apical constriction in the neural plate is controlled and how it contributes to tissue morphogenesis are not fully understood. In this study, we show that intracellular calcium ions (Ca2+) are required for Xenopus neural tube formation and that there are two types of Ca(2+)concentrationchanges, a single-cell and a multicellular wave-like fluctuation, in the developing neural plate. Quantitative imaging analyses revealed that transient increases in Ca2+ concentration induced cortical F-actin remodeling, apical constriction and accelerations of the closing movement of the neural plate. We also show that extracellular ATP and N-cadherin (cdh2) participate in the Ca2+-induced apical constriction. Furthermore, our mathematical model suggests that the effect of Ca2+ fluctuations on tissue morphogenesis is independent of fluctuation frequency and that fluctuations affecting individual cells are more efficient than those at the multicellular level. We propose that distinct Ca2+ signaling patterns differentially modulate apical constriction for efficient epithelial folding and that this mechanism has a broad range of physiological outcomes.

リンク情報
DOI
https://doi.org/10.1242/dev.141952
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000397631800017&DestApp=WOS_CPL
ID情報
  • DOI : 10.1242/dev.141952
  • ISSN : 0950-1991
  • eISSN : 1477-9129
  • Web of Science ID : WOS:000397631800017

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