Elsevier

Developmental Biology

Volume 394, Issue 2, 15 October 2014, Pages 206-216
Developmental Biology

Junctionally restricted RhoA activity is necessary for apical constriction during phase 2 inner ear placode invagination

https://doi.org/10.1016/j.ydbio.2014.08.022Get rights and content
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Highlights

  • Otic placode invagination is biphasic, basal expansion followed by apical constriction.

  • The activity of the RhoGEF, ArhGEF11 ensures the restriction of RhoA activity to apical junctions.

  • RhoA activity controls the activation of the Rho-associated protein kinase, ROCK1 and 2.

  • ROCK1/2 phosphorylates and activates myosin-II light chain.

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.

Keywords

Inner ear
Placode
Invagination
RhoA
Myosin-II
Morphogenesis

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