LymphedemaV1, Main, Exploration, bibRecord, 005F36

Zyxin Mediates Actin Fiber Reorganization in Epithelial–Mesenchymal Transition and Contributes to Endocardial Morphogenesis

Identifieur interne : 005F36 ( Main/Exploration ); précédent : 005F35; suivant : 005F37

Zyxin Mediates Actin Fiber Reorganization in Epithelial–Mesenchymal Transition and Contributes to Endocardial Morphogenesis

Auteurs : Masaki Mori ; Hironori Nakagami ; Nobutaka Koibuchi [Japon] ; Koichi Miura [Japon] ; Yoichi Takami ; Hiroshi Koriyama ; Hiroki Hayashi ; Hisataka Sabe [Japon] ; Naoki Mochizuki [Japon] ; Ryuichi Morishita [Japon] ; Yasufumi Kaneda

Source :

Molecular Biology of the Cell [ 1059-1524 ] ; 2009.

RBID : PMC:2704162

Abstract

Epithelial–mesenchymal transition (EMT) confers destabilization of cell–cell adhesion and cell motility required for morphogenesis or cancer metastasis. Here we report that zyxin, a focal adhesion-associated LIM protein, is essential for actin reorganization for cell migration in TGF-β1–induced EMT in normal murine mammary gland (NMuMG) cells. TGF-β1 induced the relocation of zyxin from focal adhesions to actin fibers. In addition, TGF-β1 up-regulated zyxin via a transcription factor, Twist1. Depletion of either zyxin or Twist1 abrogated the TGF-β1–dependent EMT, including enhanced cell motility and actin reorganization, indicating the TGF-β1-Twist1-zyxin signal for EMT. Both zyxin and Twist1 were predominantly expressed in the cardiac atrioventricular canal (AVC) that undergoes EMT during heart development. We further performed ex vivo AVC explant assay and revealed that zyxin was required for the reorganization of actin fibers and migration of the endocardial cells. Thus, zyxin reorganizes actin fibers and enhances cell motility in response to TGF-β1, thereby regulating EMT.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2704162

DOI: 10.1091/mbc.E09-01-0046
PubMed: 19439447
PubMed Central: 2704162

Affiliations:

Le document en format XML

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<front><div type="abstract" xml:lang="en"><p>Epithelial–mesenchymal transition (EMT) confers destabilization of cell–cell adhesion and cell motility required for morphogenesis or cancer metastasis. Here we report that zyxin, a focal adhesion-associated LIM protein, is essential for actin reorganization for cell migration in TGF-β1–induced EMT in normal murine mammary gland (NMuMG) cells. TGF-β1 induced the relocation of zyxin from focal adhesions to actin fibers. In addition, TGF-β1 up-regulated zyxin via a transcription factor, Twist1. Depletion of either zyxin or Twist1 abrogated the TGF-β1–dependent EMT, including enhanced cell motility and actin reorganization, indicating the TGF-β1-Twist1-zyxin signal for EMT. Both zyxin and Twist1 were predominantly expressed in the cardiac atrioventricular canal (AVC) that undergoes EMT during heart development. We further performed ex vivo AVC explant assay and revealed that zyxin was required for the reorganization of actin fibers and migration of the endocardial cells. Thus, zyxin reorganizes actin fibers and enhances cell motility in response to TGF-β1, thereby regulating EMT.</p>
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Zyxin Mediates Actin Fiber Reorganization in Epithelial–Mesenchymal Transition and Contributes to Endocardial Morphogenesis

Zyxin Mediates Actin Fiber Reorganization in Epithelial–Mesenchymal Transition and Contributes to Endocardial Morphogenesis

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Abstract

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