Involvement of extracellular matrix in the formation of the inner ear

Formation of the inner ear from the otic placode differs from invagination of other cup‐shaped organ primordia. Activation of the actin cytoskeleton seems to play a limited role because precocious invagination does not occur upon treatment with activators of a contractile event and cannot be prevent...

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Bibliographic Details
Published in:Developmental dynamics 1995-04, Vol.202 (4), p.421-432
Main Authors: Gerchman, Eric, Hilfer, S. Robert, Brown, Joyce W.
Format: Article
Language:English
Subjects:
Animals
Bacterial Proteins - pharmacology
Chick Embryo
Chondroitin Lyases - pharmacology
Chondroitin sulfate
Ear, Inner - embryology
Embryonic Induction - drug effects
Enzyme injection
Extracellular matrix
Extracellular Matrix - drug effects
Extracellular Matrix - physiology
Glycosaminoglycans - metabolism
Glycosides - pharmacology
Hyaluronate
Hyaluronoglucosaminidase - pharmacology
Image Processing, Computer-Assisted
Mesoderm - drug effects
Mesoderm - metabolism
Microinjections
Morphogenesis
Organogenesis
Otic vesicle
β‐xyloside
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Summary:Formation of the inner ear from the otic placode differs from invagination of other cup‐shaped organ primordia. Activation of the actin cytoskeleton seems to play a limited role because precocious invagination does not occur upon treatment with activators of a contractile event and cannot be prevented by inhibitors. In this study, the possibility that invagination is mediated by changes in the surrounding mesenchyme was tested by treating embryos with agents which interfere with the integrity of extracellular matrix. Enzymes degrading hyaluronate and/or chondroitin sulfate were microinjected into the otic region prior to folding. Synthesis of chondroitin sulfate proteoglycan was inhibited by microinjection of β‐xyloside. All treatment inhibited otic pit formation by interfering with fold formation within the placode. Immunocytochemical procedures showed depletion of the appropriate extracellular matrix components for a short time period after enzyme treatments and for up to 24 hr after β‐xyloside injection. Invagination of the otic primordium is concluded to be controlled in part by anchorage of the epithelium to adjacent structures and possibly by expansion of the mesenchymal extracellular matrix. © 1995 Wiley‐Liss, Inc.
ISSN:1058-8388
1097-0177
DOI:10.1002/aja.1002020411