title: Epibranchial and otic placodes are induced by a common Fgf signal, but their subsequent development is independent.
abstract: The epibranchial placodes are cranial, ectodermal thickenings that give rise to sensory neurons of the peripheral nervous system. Despite their importance in the developing animal, the signals responsible for their induction remain unknown. Using the placodal marker, sox3, we have shown that the same Fgf signaling required for otic vesicle development is required for the development of the epibranchial placodes. Loss of both Fgf3 and Fgf8 is sufficient to block placode development. We further show that epibranchial sox3 expression is unaffected in mutants in which no otic placode forms, where dlx3b and dlx4b are knocked down, or deleted along with sox9a. However, the forkhead factor, Foxi1, is required for both otic and epibranchial placode development. Thus, both the otic and epibranchial placodes form in a common region of ectoderm under the influence of Fgfs, but these two structures subsequently develop independently. Although previous studies have investigated the signals that trigger neurogenesis from the epibranchial placodes, this represents the first demonstration of the signaling events that underlie the formation of the placodes themselves, and therefore, the process that determines which ectodermal cells will adopt a neural fate.
authors.affiliation: Children's Brain Tumour Research Centre, Institute of Genetics, Queen's Medical Centre, University of Nottingham, Nottingham, NG7 2UH, UK.
authors.forename: Shun-Kuo
authors.initials: SK
authors.lastname: Sun
authors.forename: Chris T
authors.initials: CT
authors.lastname: Dee
authors.forename: Vineeta B
authors.initials: VB
authors.lastname: Tripathi
authors.forename: Andrea
authors.initials: A
authors.lastname: Rengifo
authors.forename: Caroline S
authors.initials: CS
authors.lastname: Hirst
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Scotting
mesh_terms: D000818:Animals; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D004475:Ectoderm / Q000166:cytology / Q000378:metabolism; D051518:Fibroblast Growth Factor 3 / Q000235:genetics / Q000378:metabolism; D005346:Fibroblast Growth Factors / Q000235:genetics / Q000378:metabolism*; D051858:Forkhead Transcription Factors / Q000235:genetics / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental; D006609:High Mobility Group Proteins / Q000235:genetics / Q000378:metabolism; D017403:In Situ Hybridization; D008954:Models, Biological; D009154:Mutation; D009475:Neurons, Afferent / Q000166:cytology / Q000378:metabolism; D010525:Peripheral Nerves / Q000196:embryology* / Q000378:metabolism*; D055748:SOXB1 Transcription Factors; D015398:Signal Transduction; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism; D015027:Zebrafish / Q000196:embryology* / Q000235:genetics / Q000378:metabolism*; D029961:Zebrafish Proteins / Q000235:genetics / Q000378:metabolism*
chemical_list: D004268:DNA-Binding Proteins; D051518:Fibroblast Growth Factor 3; D051858:Forkhead Transcription Factors; D006609:High Mobility Group Proteins; D055748:SOXB1 Transcription Factors; D014157:Transcription Factors; D029961:Zebrafish Proteins; C489200:fgf3 protein, zebrafish; C517774:fgf8a protein, zebrafish; C472802:foxi1 protein, zebrafish; D005346:Fibroblast Growth Factors