A Fate Map of Chick Otic Cup Closure Reveals Lineage Boundaries in the Dorsal Otocyst

The vertebrate inner ear is structurally complex, consisting of fluid-filled tubules and sensory organs that subserve the functions of hearing and balance. The epithelial parts of the inner ear are derived from the otic placode, which deepens to form a cup before closing to form the otic vesicle. We...

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Bibliographic Details
Published in:Developmental biology 2000-11, Vol.227 (2), p.256-270
Main Authors: Brigande, John V., Iten, Laurie E., Fekete, Donna M.
Format: Article
Language:English
Subjects:
Animals
Body Patterning
Chick Embryo
Ear, Inner - embryology
Ear, Inner - metabolism
endolymphatic duct
fate map
Fluorescent Dyes - administration & dosage
Gene Expression Regulation, Developmental
inner ear
lineage boundary
Models, Biological
otic cup
Time Factors
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Summary:The vertebrate inner ear is structurally complex, consisting of fluid-filled tubules and sensory organs that subserve the functions of hearing and balance. The epithelial parts of the inner ear are derived from the otic placode, which deepens to form a cup before closing to form the otic vesicle. We fate-mapped the rim of the otic cup to monitor the cellular movements associated with otocyst formation and to aid in interpreting the changing gene expression patterns of the early otic field. Twelve sites around the rim, defined as positions of a clock face, were targeted by iontophoretic injection of fluorescent, lipophilic dye. Labeled cells were imaged 24 and 48 h after injection. The data show that the entire dorsal rim of the otic cup becomes the endolymphatic duct (ED), while the posteroventral rim becomes the lateral otocyst wall. Two intersecting boundaries of lineage restriction were identified near the dorsal pole: one bisecting the ED into anterior and posterior halves and the other defining its lateral edge. We hypothesize that signaling across compartment boundaries may play a critical role in duct specification. This model is discussed in the context of mouse mutants that are defective in both hindbrain development and ED outgrowth.
ISSN:0012-1606
1095-564X
DOI:10.1006/dbio.2000.9914