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Semin Cell Dev Biol
2017 May 01;65:39-46. doi: 10.1016/j.semcdb.2016.10.006.
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Changing shape and shaping change: Inducing the inner ear.
Ladher RK
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The inner ear arises from non-neural ectoderm as a result of instructions sent by surrounding tissues. These interactions progressively restrict the potential of the ectoderm, resulting in the formation of the otic placode, a disk of thickened ectoderm that will give rise to all of the inner ear derivatives and its neurons. While otic placode is a surface structure, the inner ear is internalised, embedded within the cranial mesenchyme. Here, the cellular and molecular interactions that restrict the lineage of non-neural ectoderm in its transition to otic placode are reviewed, and how these interactions impinge on the coordination of otic placodal cell shape that drive the dramatic morphogenesis of the placode, as it becomes the otocyst.
Fig. 1. Induction of the Inner Ear.
Diagram showing the role moelcular and cellular interactions play in the restriction of ectoderm into otic fated cells. OEPD induction occurs during neurulation where FGF signals emanating from the mesoderm (grey) act on both the overlying pre-placodal region tissue (pink) to induce the otic-epibranchial placodal domain, and the overlying neural tissue to induce Wnt8a (green). Otic induction occurs when Wnt8a together with Fgf3 acts on the OEPD to specify otic placode cells (purple) from the OEPD whilst suppressing epibranchial placodal cells. Modified from Sai and Ladher [9].
Fig. 2. Diagram depicting the invagination of the inner ear.
Thickened placodal ectoderm begins to invaginate at HH10/10ss (somite stage) by basal expansion. This is followed at HH12/16ss by apical constriction. The consecutive activities cause progressive deepening of the otic placode, so it forms an otic cup. At around HH15 to HH16, the otic cup closes, pinching off from the surface ectoderm.
Fig. 3. Model showing control of Phase 1 and Phase 2 otic invagination.
Shown are cells undergoing phase 1 (A) and phase 2 (B) otic invagination.
(A) Shown is apical actin (green stripe) found within the apical junctional region (yellow). This area is devoid of active myosin-II. This is found on the basal side of the cell (red). Myosin-II is activated by the action of basal FGF acting on its receptor, triggering a cascade via phospholipase C gamma (PLCγ) and protein kinase C alpha (PKCα) which results in the phosphorylation of myosin light chain (MLC). Active myosin-II results in the depolymerization of basal actin [72]. (B) Phase 2 morphogenesis is characterised by the co-localization of actin and activate myosin-II in the apical junctional region. The phosphorylation of MLC results from the activation of RhoA by the Gef, ArhGef11[71]. Figure adapted from Sai et al. [71].
