Morphogenesis of the Inner Ear

Mansour, Suzanne L.; Schoenwolf, Gary C.

doi:10.1007/0-387-30678-1_3

Cited by 22 publications

(25 citation statements)

References 176 publications

(193 reference statements)

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“…Tissue ablation and transplantation studies, as well as observations of classic and targeted mutants, show that these tissues are necessary and sufficient for induction of otic placode gene expression and for induction of placodal morphology and subsequent development (for reviews, see Baker and Bronner-Fraser 2001;Kiernan et al 2002;Riley and Phillips 2003). FGF signals are clearly required for the earliest stages of otic induction as well as for subsequent development of the otic placode and vesicle (for reviews, see Riley and Phillips 2003;Wright and Mansour 2003b;Mansour and Schoenwolf 2005). The four major vertebrate models (Xenopus, zebrafish, chick, and mouse) all express Fgf3 in dorsal neural ectoderm adjacent to preplacodal tissue (Wilkinson et al 1988;Tannahill et al 1992;Mahmood et al 1995;Raible and Brand 2001), and at least in zebrafish and mice, an FGF3 signal is required (redundantly with another FGF signal) for induction of the otic placode.…”

Section: The Tissue Sources Of Fgf Signals Potentially Relevant For Imentioning

confidence: 99%

FGF8 initiates inner ear induction in chick and mouse

Ladher¹,

Wright²,

Moon³

et al. 2005

Genes Dev.

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In both chick and mouse, the otic placode, the rudiment of the inner ear, is induced by at least two signals, one from the cephalic paraxial mesoderm and the other from the neural ectoderm. In chick, the mesodermal signal, FGF19, induces neural ectoderm to express additional signals, including WNT8c and FGF3, resulting in induction of the otic placode. In mouse, mesodermal Fgf10 acting redundantly with neural Fgf3 is required for induction of the placode. To determine how the mesodermal inducers of the otic placode are localized, we took advantage of the unique strengths of the two model organisms. We show that endoderm is necessary for otic induction in the chick and that Fgf8, expressed in the chick endoderm subjacent to Fgf19, is both sufficient and necessary for the expression of Fgf19 in the mesoderm. In the mouse, Fgf8 is also expressed in endoderm as well as in other germ layers in the periotic placode region. We show that otic induction fails in embryos null for Fgf3 and hypomorphic for Fgf8 and expression of mesodermal Fgf10 is reduced. Thus, Fgf8 plays a critical upstream role in an FGF signaling cascade required for otic induction in chick and mouse.

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Section: The Tissue Sources Of Fgf Signals Potentially Relevant For Imentioning

confidence: 99%

FGF8 initiates inner ear induction in chick and mouse

Ladher¹,

Wright²,

Moon³

et al. 2005

Genes Dev.

Self Cite

183

230

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“…During this period, there are additional evaginations of the central region to form the more dorsally situated utricle and the more ventrally situated saccule. By E15.5, the inner ear epithelium has acquired its mature morphology, but is still undergoing cellular differentiation within the six sensory patches (Kiernan et al, 2002;Barald and Kelley, 2004;Mansour and Schoenwolf, 2005;Fritzsch et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Fgf3is required for dorsal patterning and morphogenesis of the inner ear epithelium

et al. 2007

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The inner ear, which contains sensory organs specialized for hearing and balance, develops from an ectodermal placode that invaginates lateral to hindbrain rhombomeres (r) 5-6 to form the otic vesicle. Under the influence of signals from intra-and extraotic sources, the vesicle is molecularly patterned and undergoes morphogenesis and cell-type differentiation to acquire its distinct functional compartments. We show in mouse that Fgf3, which is expressed in the hindbrain from otic induction through endolymphatic duct outgrowth, and in the prospective neurosensory domain of the otic epithelium as morphogenesis initiates, is required for both auditory and vestibular function. We provide new morphologic data on otic dysmorphogenesis in Fgf3 mutants, which show a range of malformations similar to those of Mafb (Kreisler), Hoxa1 and Gbx2 mutants, the most common phenotype being failure of endolymphatic duct and common crus formation, accompanied by epithelial dilatation and reduced cochlear coiling. The malformations have close parallels with those seen in hearing-impaired patients. The morphologic data, together with an analysis of changes in the molecular patterning of Fgf3 mutant otic vesicles, and comparisons with other mutations affecting otic morphogenesis, allow placement of Fgf3 between hindbrain-expressed Hoxa1 and Mafb, and otic vesicle-expressed Gbx2, in the genetic cascade initiated by WNT signaling that leads to dorsal otic patterning and endolymphatic duct formation. Finally, we show that Fgf3 prevents ventral expansion of r5-6 neurectodermal Wnt3a, serving to focus inductive WNT signals on the dorsal otic vesicle and highlighting a new example of cross-talk between the two signaling systems.

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“…Through a complicated embryogenesis influenced by numerous autocrine and paracrine factors, the surrounding mesenchyme undergoes chondrogenesis, which will eventually form the bony capsule that encircles the membranous labyrinth. [12][13][14][15] The mechanism of ossification of the OC is mainly by EO, with intrachondral bone ossification predominating in some stages. 16 Histologically, the ossifying OC has 3 layers: a thin inner (endosteal) layer, a middle layer composed of a combination of endochondral and intrachondral bone, and an outer (periosteal) layer.…”

Section: Discussionmentioning

confidence: 99%