論文

査読有り 筆頭著者 責任著者
2016年11月

DAAM1 stabilizes epithelial junctions by restraining WAVE complex-dependent lateral membrane motility

Journal of Cell Biology
  • Tamako Nishimura
  • ,
  • Shoko Ito
  • ,
  • Hiroko Saito
  • ,
  • Sylvain Hiver
  • ,
  • Kenta Shigetomi
  • ,
  • Junichi Ikenouchi
  • ,
  • Masatoshi Takeichi

215
4
開始ページ
559
終了ページ
573
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1083/jcb.201603107
出版者・発行元
ROCKEFELLER UNIV PRESS

Epithelial junctions comprise two subdomains, the apical junctional complex (AJC) and the adjacent lateral membrane contacts (LCs), that span the majority of the junction. The AJC is lined with circumferential actin cables, whereas the LCs are associated with less-organized actin filaments whose roles are elusive. We found that DAAM1, a formin family actin regulator, accumulated at the LCs, and its depletion caused dispersion of actin filaments at these sites while hardly affecting circumferential actin cables. DAAM1 loss enhanced the motility of LC-forming membranes, leading to their invasion of neighboring cell layers, as well as disruption of polarized epithelial layers. We found that components of the WAVE complex and its downstream targets were required for the elevation of LC motility caused by DAAM1 loss. These findings suggest that the LC membranes are motile by nature because of the WAVE complex, but DAAM1-mediated actin regulation normally restrains this motility, thereby stabilizing epithelial architecture, and that DAAM1 loss evokes invasive abilities of epithelial cells.

リンク情報
DOI
https://doi.org/10.1083/jcb.201603107
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/27807130
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000388690900013&DestApp=WOS_CPL
ID情報
  • DOI : 10.1083/jcb.201603107
  • ISSN : 0021-9525
  • eISSN : 1540-8140
  • PubMed ID : 27807130
  • Web of Science ID : WOS:000388690900013

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