Junctionally restricted RhoA activity is necessary for apical constriction during phase 2 inner ear placode invagination
Autor: | Raj K. Ladher, Xiaorei Sai, Shigenobu Yonemura |
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Rok vydání: | 2014 |
Předmět: |
RHOA
Blotting Western Morphogenesis Chick Embryo Naphthalenes Heterocyclic Compounds 4 or More Rings Image Processing Computer-Assisted medicine Animals Inner ear Otic placode Molecular Biology Rho-associated protein kinase Actin rho-Associated Kinases biology Gene Expression Regulation Developmental Apical constriction Azepines Cell Biology Cadherins Immunohistochemistry Epithelium Cell biology Electroporation medicine.anatomical_structure Ear Inner biology.protein RNA Interference sense organs Peptides rhoA GTP-Binding Protein Developmental Biology |
Zdroj: | Developmental Biology. 394:206-216 |
ISSN: | 0012-1606 |
DOI: | 10.1016/j.ydbio.2014.08.022 |
Popis: | After induction, the inner ear is transformed from a superficially located otic placode into an epithelial vesicle embedded in the mesenchyme of the head. Invagination of this epithelium is biphasic: phase 1 involves the expansion of the basal aspect of the otic cells, and phase 2, the constriction of their apices. Apical constriction is important not only for otic invagination, but also the invagination of many other epithelia; however, its molecular basis is still poorly understood. Here we show that phase 2 otic morphogenesis, like phase 1 morphogenesis, results from the activation of myosin-II. However unlike the actin depolymerising activity observed basally, active myosin-II results in actomyosin contractility. Myosin-II activation is triggered by the accumulation of the planar cell polarity (PCP) core protein, Celsr1 in apical junctions (AJ). Apically polarized Celsr1 orients and recruits the Rho Guanine exchange factor (GEF) ArhGEF11 to apical junctions, thus restricting RhoA activity to the junctional membrane where it activates the Rho kinase ROCK. We suggest that myosin-II and RhoA activation results in actomyosin dependent constriction in an apically polarised manner driving otic epithelium invagination. |
Databáze: | OpenAIRE |
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