A role for neural cell adhesion molecule in the formation of the avian inner ear

Brown, Joyce; Beck‐Jefferson, Ernestine; Hilfer, S. Robert

doi:10.1002/(sici)1097-0177(199812)213:4<359::aid-aja2>3.0.co;2-2

Cited by 9 publications

(3 citation statements)

References 32 publications

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“…Close attachment of otic cup epithelium to neural tube basal lamina is thought to be necessary for normal invagination in chicken embryos (Brown et al, 1998;Moro-Balbás et al, 2000;Visconti and Hilfer, 2002). Mouse Gata3 starts to be expressed in otic placode around the time when it starts to invaginate and we show here that it controls the earliest otic morphogenetic steps.…”

Section: Aberrant Otic Placode Invagination and Formation Of An Ectopmentioning

confidence: 51%

Gata3 is required for early morphogenesis and Fgf10 expression during otic development

Lilleväli

Haugas

Matilainen

et al. 2006

Mechanisms of Development

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Inner ear develops from an induced surface ectoderm placode that invaginates and closes to form the otic vesicle, which then undergoes a complex morphogenetic process to form the membranous labyrinth. Inner ear morphogenesis is severely affected in Gata3 deficient mouse embryos, but the onset and basis of the phenotype has not been known. We show here that Gata3 deficiency leads to severe and unique abnormalities during otic placode invagination. The invagination problems are accompanied often by the formation of a morphological boundary between the dorsal and ventral otic cup and by the precocious appearance of dorsal endolymphatic characteristics. In addition, the endolymphatic domain often detaches from the rest of the otic epithelium during epithelial closure. The expression of several cell adhesion mediating genes is altered in Gata3 deficient ears suggesting that Gata3 controls adhesion and morphogenetic movements in early otic epithelium. Inactivation of Gata3 leads also to a loss of Fgf10 expression in otic epithelium and auditory ganglion demonstrating that Gata3 is an important regulator of Fgf-signalling during otic development.

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Section: Aberrant Otic Placode Invagination and Formation Of An Ectopmentioning

confidence: 51%

Gata3 is required for early morphogenesis and Fgf10 expression during otic development

Lilleväli

Haugas

Matilainen

et al. 2006

Mechanisms of Development

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“…Recently Brown et al (1998) demonstrated that in avian embryos microinjection of blocking antibodies to N-CAM into the paraxial mesoderm adjacent to the otic placode resulted in two major classes of defects: detachment of the primordium from the neural tube and interference with formation of the otic folds. It is known that HSPG may interact with N-CAM at plasmatic membrane level (Cole and Burg 1989) and this interaction might produce changes in N-CAM structure that modulate cellular adhesion, thereby facilitating epithelial folding.…”

Section: Discussionmentioning

confidence: 99%

Basal lamina heparan sulphate proteoglycan is involved in otic placode invagination in chick embryos

Moro-Balbás

Gato

Alonso

et al. 2000

Anatomy and Embryology

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Formation of the otocyst from the otic placode appears to differ from invagination of other cup-shaped organ primordia. It is known that the cellular cytoskeleton plays a limited role in otic placode invagination, whilst the extracellular matrix underlying the otic primordium intervenes in the folding process. In this study we have analysed the role of the basal lamina heparan sulphate proteoglycan in otic primordium invagination. At 10 H.H. stage, heparan sulphate proteoglycan immunomarking begins to appear on the otic placode basal lamina, increasing noticeably at 13 H.H. stage, coinciding with maximum folding of the otic epithelium, and is still present at later stages. Enzyme degradation of heparan sulphate proteoglycan in the otic primordium basal lamina, by means of microinjection with heparinase III prior to folding, significantly disrupts invagination of the otic placode, which remains practically flat, with a significant reduction in the depth of the otic pit and an increase in the diameter of the otic opening. The immunocytochemistry analysis revealed a notable depletion of basal lamina heparan sulphate proteoglycan in the otic primordia microinjected with heparinase, with no statistically significant differences observed in the volume or rate of cell proliferation in the otic epithelium relative to the control, which suggests that heparan sulphate proteoglycan disruption does not interfere with the epithelial growth. In addition, a study of apoptosis distribution by the TUNEL method confirmed that treatment with heparinase does not cause interference with cell survival in the otic epithelium. Our findings support the theory that otic primordium invagination may be regulated, at least in part, by the basal lamina components, which might contribute towards anchoring the otic epithelium to adjacent structures.

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“…In the CKO embryos, clearance of ␤-catenin protein from adherens junctions by E9.0 leads to secondary morphological defects in the remnants of the otic placode. As otic vesicle invagination is driven in part by contacts with the neural tube (Brown et al, 1998;Gerchman et al, 1995;Moro-Balbas et al, 2000;Visconti and Hilfer, 2002), it is likely that physical constraints prevent the greatly expanded placode of cAct embryos from invaginating to form an enlarged otic vesicle.…”

Section: Wnt Signaling Mediates a Cell Fate Decision Between Otic Plamentioning

confidence: 99%

Wnt signals mediate a fate decision between otic placode and epidermis

et al. 2006

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The otic placode, the anlagen of the inner ear, develops from an ectodermal field characterized by expression of the transcription factor Pax2. Previous fate mapping studies suggest that these Pax2 + cells will give rise to both otic placode tissue and epidermis, but the signals that divide the Pax2 + field into placodal and epidermal territories are unknown. We report that Wnt signaling is normally activated in a subset of Pax2 + cells, and that conditional inactivation of ␤-catenin in these cells causes an expansion of epidermal markers at the expense of the otic placode. Conversely, conditional activation of ␤-catenin in Pax2 + cells causes an expansion of the otic placode at the expense of epidermis, and the resulting otic tissue expresses exclusively dorsal otocyst markers. Together, these results suggest that Wnt signaling acts instructively to direct Pax2 + cells to an otic placodal, rather than an epidermal, fate and promotes dorsal cell identities in the otocyst.

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A role for neural cell adhesion molecule in the formation of the avian inner ear

Cited by 9 publications

References 32 publications

Gata3 is required for early morphogenesis and Fgf10 expression during otic development

Gata3 is required for early morphogenesis and Fgf10 expression during otic development

Basal lamina heparan sulphate proteoglycan is involved in otic placode invagination in chick embryos

Wnt signals mediate a fate decision between otic placode and epidermis

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