論文

査読有り
2011年1月

Development of Ca2+ signaling mechanisms and cell motility in presumptive ectodermal cells during amphibian gastrulation

DEVELOPMENT GROWTH & DIFFERENTIATION
  • Kazuhiro Takano
  • ,
  • Shuichi Obata
  • ,
  • Shinji Komazaki
  • ,
  • Mika Masumoto
  • ,
  • Tsutomu Oinuma
  • ,
  • Yuzuru Ito
  • ,
  • Takashi Ariizumi
  • ,
  • Hiroaki Nakamura
  • ,
  • Makoto Asashima

53
1
開始ページ
37
終了ページ
47
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1111/j.1440-169X.2010.01220.x
出版者・発行元
WILEY-BLACKWELL

This study investigated the development of Ca2+ signaling mechanisms and their role in initiating morphogenetic cell movement in the presumptive ectoderm of Japanese newt (Cynops pyrrhogaster) during gastrulation. Histochemical staining using fluorescently labeled ryanodine and dihydropyridine probes revealed that dihydropyridine receptor (L-type Ca2+ channels) appeared in stage 12b embryos, while ryanodine receptors were expressed in both stage 11 and 12b embryos. Transmission electron microscopy of stage 12b embryos showed abundant peripheral couplings, which are couplings of the endoplasmic reticulum and cell membrane with an approximate 12 nm gap. Caffeine increased the intracellular free Ca2+ concentration ([Ca2+](i)) in presumptive ectodermal cells isolated from both stage 11 and 12b embryos, while (+/-)-Bay K 8644 ((+/-)-BayK) increased [Ca2+](i) in cells isolated from stage 12b embryos, but not in cells isolated from stage 11 embryos. Dantrolene and nifedipine completely inhibited increases in [Ca2+](i) after treatment with caffeine and (+/-)-BayK, respectively. Caffeine activated the motility of cells isolated from both stage 11 and 12b embryos, but (+/-)-BayK only activated the motility of cells isolated from stage 12b embryos. These findings suggested that formation of the Ca2+-induced Ca2+ release system in presumptive ectodermal cells during gastrulation plays an important role in the initiation and execution of epibolic extension.

リンク情報
DOI
https://doi.org/10.1111/j.1440-169X.2010.01220.x
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000286597800005&DestApp=WOS_CPL
ID情報
  • DOI : 10.1111/j.1440-169X.2010.01220.x
  • ISSN : 0012-1592
  • Web of Science ID : WOS:000286597800005

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