Cargando…

Nodal signaling regulates endodermal cell motility and actin dynamics via Rac1 and Prex1

Embryo morphogenesis is driven by dynamic cell behaviors, including migration, that are coordinated with fate specification and differentiation, but how such coordination is achieved remains poorly understood. During zebrafish gastrulation, endodermal cells sequentially exhibit first random, nonpers...

Descripción completa

Detalles Bibliográficos
Autores principales: Woo, Stephanie, Housley, Michael P., Weiner, Orion D., Stainier, Didier Y.R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3432772/
https://www.ncbi.nlm.nih.gov/pubmed/22945937
http://dx.doi.org/10.1083/jcb.201203012
_version_ 1782242243921313792
author Woo, Stephanie
Housley, Michael P.
Weiner, Orion D.
Stainier, Didier Y.R.
author_facet Woo, Stephanie
Housley, Michael P.
Weiner, Orion D.
Stainier, Didier Y.R.
author_sort Woo, Stephanie
collection PubMed
description Embryo morphogenesis is driven by dynamic cell behaviors, including migration, that are coordinated with fate specification and differentiation, but how such coordination is achieved remains poorly understood. During zebrafish gastrulation, endodermal cells sequentially exhibit first random, nonpersistent migration followed by oriented, persistent migration and finally collective migration. Using a novel transgenic line that labels the endodermal actin cytoskeleton, we found that these stage-dependent changes in migratory behavior correlated with changes in actin dynamics. The dynamic actin and random motility exhibited during early gastrulation were dependent on both Nodal and Rac1 signaling. We further identified the Rac-specific guanine nucleotide exchange factor Prex1 as a Nodal target and showed that it mediated Nodal-dependent random motility. Reducing Rac1 activity in endodermal cells caused them to bypass the random migration phase and aberrantly contribute to mesodermal tissues. Together, our results reveal a novel role for Nodal signaling in regulating actin dynamics and migration behavior, which are crucial for endodermal morphogenesis and cell fate decisions.
format Online
Article
Text
id pubmed-3432772
institution National Center for Biotechnology Information
language English
publishDate 2012
publisher The Rockefeller University Press
record_format MEDLINE/PubMed
spelling pubmed-34327722013-03-03 Nodal signaling regulates endodermal cell motility and actin dynamics via Rac1 and Prex1 Woo, Stephanie Housley, Michael P. Weiner, Orion D. Stainier, Didier Y.R. J Cell Biol Research Articles Embryo morphogenesis is driven by dynamic cell behaviors, including migration, that are coordinated with fate specification and differentiation, but how such coordination is achieved remains poorly understood. During zebrafish gastrulation, endodermal cells sequentially exhibit first random, nonpersistent migration followed by oriented, persistent migration and finally collective migration. Using a novel transgenic line that labels the endodermal actin cytoskeleton, we found that these stage-dependent changes in migratory behavior correlated with changes in actin dynamics. The dynamic actin and random motility exhibited during early gastrulation were dependent on both Nodal and Rac1 signaling. We further identified the Rac-specific guanine nucleotide exchange factor Prex1 as a Nodal target and showed that it mediated Nodal-dependent random motility. Reducing Rac1 activity in endodermal cells caused them to bypass the random migration phase and aberrantly contribute to mesodermal tissues. Together, our results reveal a novel role for Nodal signaling in regulating actin dynamics and migration behavior, which are crucial for endodermal morphogenesis and cell fate decisions. The Rockefeller University Press 2012-09-03 /pmc/articles/PMC3432772/ /pubmed/22945937 http://dx.doi.org/10.1083/jcb.201203012 Text en © 2012 Woo et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
spellingShingle Research Articles
Woo, Stephanie
Housley, Michael P.
Weiner, Orion D.
Stainier, Didier Y.R.
Nodal signaling regulates endodermal cell motility and actin dynamics via Rac1 and Prex1
title Nodal signaling regulates endodermal cell motility and actin dynamics via Rac1 and Prex1
title_full Nodal signaling regulates endodermal cell motility and actin dynamics via Rac1 and Prex1
title_fullStr Nodal signaling regulates endodermal cell motility and actin dynamics via Rac1 and Prex1
title_full_unstemmed Nodal signaling regulates endodermal cell motility and actin dynamics via Rac1 and Prex1
title_short Nodal signaling regulates endodermal cell motility and actin dynamics via Rac1 and Prex1
title_sort nodal signaling regulates endodermal cell motility and actin dynamics via rac1 and prex1
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3432772/
https://www.ncbi.nlm.nih.gov/pubmed/22945937
http://dx.doi.org/10.1083/jcb.201203012
work_keys_str_mv AT woostephanie nodalsignalingregulatesendodermalcellmotilityandactindynamicsviarac1andprex1
AT housleymichaelp nodalsignalingregulatesendodermalcellmotilityandactindynamicsviarac1andprex1
AT weineroriond nodalsignalingregulatesendodermalcellmotilityandactindynamicsviarac1andprex1
AT stainierdidieryr nodalsignalingregulatesendodermalcellmotilityandactindynamicsviarac1andprex1