Junctionally restricted RhoA activity is necessary for apical constriction during phase 2 inner ear placode invagination.
Dev Biol
; 394(2): 206-16, 2014 Oct 15.
Article
en En
| MEDLINE
| ID: mdl-25173873
ABSTRACT
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.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Regulación del Desarrollo de la Expresión Génica
/
Proteína de Unión al GTP rhoA
/
Oído Interno
/
Morfogénesis
Límite:
Animals
Idioma:
En
Revista:
Dev Biol
Año:
2014
Tipo del documento:
Article
País de afiliación:
Japón