z-logo
Premium
FilaminB is required for the directed localization of cell–cell adhesion molecules in embryonic epithelial development
Author(s) -
Wakamatsu Yoshio,
Sakai Daisuke,
Suzuki Takashi,
Osumi Noriko
Publication year - 2011
Publication title -
developmental dynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.634
H-Index - 141
eISSN - 1097-0177
pISSN - 1058-8388
DOI - 10.1002/dvdy.22518
Subject(s) - filamin , microbiology and biotechnology , biology , neural tube , epithelium , cadherin , cell adhesion molecule , cell adhesion , embryonic stem cell , actin , gene knockdown , neural cell adhesion molecule , cell , embryo , cytoskeleton , cell culture , biochemistry , genetics , gene
Filamin proteins cross‐link F‐actin and form a scaffold for numerous signal transduction systems. In this study, we show that filaminB is apically enriched in avian embryonic epithelium, and colocalizes with cell adhesion molecules and circumferential F‐actin. FilaminB knockdown in the neural tube and somites decreases the accumulation of N‐cadherin and ZO‐1 protein at cell junctions, and promotes disruption of these tissues and the presence of neuronal aggregates within the lumen of the neural tube. This phenotype resembles that of human congenital condition, periventricular heterotopia (PH). FilaminB knockdown in MDCK cells suggests that filaminB is required for the apical accumulation of adhesion molecules in the junctional complex and subsequent epithelium formation. We further suggest that the reduction of structural integrity of the neural epithelium caused by the loss of Filamin function may also result in formation of the neuronal nodules found in PH patients. Developmental Dynamics, 2011. © 2010 Wiley‐Liss, Inc.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here