Morphogenesis of the primitive gut tube is generated by Rho/ROCK/myosin IIâmediated endoderm rearrangements
Autor: | Rachel A. Reed, Nanette Nascone-Yoder, Allison R. Morckel, Michel K. Dush, Mandy Womble, E. W. Devlin, Stephanie Bloom, Rhesa R. Tull |
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Rok vydání: | 2009 |
Předmět: |
Embryo
Nonmammalian Gastrointestinal Diseases Xenopus Morphogenesis Organogenesis Biology Models Biological Animals Genetically Modified Myosin medicine Animals Cell Shape Body Patterning Genetics rho-Associated Kinases Nonmuscle Myosin Type IIB Endoderm Cell Polarity Gastrula biology.organism_classification Epithelium Cell biology Gastrointestinal Tract Gastrulation medicine.anatomical_structure Elongation rhoA GTP-Binding Protein Signal Transduction Developmental Biology |
Zdroj: | Developmental Dynamics. 238:3111-3125 |
ISSN: | 1097-0177 1058-8388 |
DOI: | 10.1002/dvdy.22157 |
Popis: | During digestive organogenesis, the primitive gut tube (PGT) undergoes dramatic elongation and forms a lumen lined by a single-layer of epithelium. In Xenopus, endoderm cells in the core of the PGT rearrange during gut elongation, but the morphogenetic mechanisms controlling their reorganization are undetermined. Here, we define the dynamic changes in endoderm cell shape, polarity, and tissue architecture that underlie Xenopus gut morphogenesis. Gut endoderm cells intercalate radially, between their anterior and posterior neighbors, transforming the nearly solid endoderm core into a single layer of epithelium while concomitantly eliciting “radially convergent” extension within the gut walls. Inhibition of Rho/ROCK/Myosin II activity prevents endoderm rearrangements and consequently perturbs both gut elongation and digestive epithelial morphogenesis. Our results suggest that the cellular and molecular events driving tissue elongation in the PGT are mechanistically analogous to those that function during gastrulation, but occur within a novel cylindrical geometry to generate an epithelial-lined tube. Developmental Dynamics 238:3111–3125, 2009. © 2009 Wiley-Liss, Inc. |
Databáze: | OpenAIRE |
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