TY - CHAP
T1 - Development of the Pre-Placodal Ectoderm and Cranial Sensory Placodes
AU - Moody, Sally A.
AU - Saint-Jeannet, Jean Pierre
N1 - Funding Information:
We apologize to those authors whose work was not cited due to space limitations. Work from the authors’ laboratories is supported by NIH grant R01 DE022065 (S. A. M.) and R01 DE014212 (J-P. S-J.) We wish to thank members of the Moody and Saint-Jeannet labs for helpful comments on the manuscript.
Publisher Copyright:
© 2015 Elsevier Inc. All rights reserved.
Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 2015
Y1 - 2015
N2 - Cranial sensory placodes arise from a common precursor field, the pre-placodal ectoderm (PPE), which surrounds the anterior neural plate just lateral to the neural crest. They give rise to secretory cells and numerous sensory structures in the vertebrate head. The PPE forms in response to interactions between the neural and non-neural ectoderm and to signaling factors (FGF, BMP, Wnt and retinoic acid) from adjacent tissues (underlying mesoderm, endoderm, anterior neural ridge). Members of the Six family of transcription factors, particularly Six1 and Six4, are major regulators of PPE fate specification. Six1 upregulates other placode genes and downregulates epidermal and neural crest genes, thus maintaining PPE/placodal fate. Several co-factor proteins, including members of the Eya, Groucho and Dachund families, modify Six protein activity. The PPE is initially competent to form all of the different placodes. Signaling from adjacent tissues along its anterior-posterior extent activates different sets of transcription factors that cause the PPE to separate into individual placodes with different developmental fates. Six1 and Eya1 maintain placode cells in an undifferentiated, proliferative state. They are downregulated when differentiation is initiated. For placode-derived neurons, this involves a dose-dependent regulation of SoxB1 transcription factors. Mutations in SIX and EYA genes underlie several human syndromes whose phenotypes often include hearing loss.
AB - Cranial sensory placodes arise from a common precursor field, the pre-placodal ectoderm (PPE), which surrounds the anterior neural plate just lateral to the neural crest. They give rise to secretory cells and numerous sensory structures in the vertebrate head. The PPE forms in response to interactions between the neural and non-neural ectoderm and to signaling factors (FGF, BMP, Wnt and retinoic acid) from adjacent tissues (underlying mesoderm, endoderm, anterior neural ridge). Members of the Six family of transcription factors, particularly Six1 and Six4, are major regulators of PPE fate specification. Six1 upregulates other placode genes and downregulates epidermal and neural crest genes, thus maintaining PPE/placodal fate. Several co-factor proteins, including members of the Eya, Groucho and Dachund families, modify Six protein activity. The PPE is initially competent to form all of the different placodes. Signaling from adjacent tissues along its anterior-posterior extent activates different sets of transcription factors that cause the PPE to separate into individual placodes with different developmental fates. Six1 and Eya1 maintain placode cells in an undifferentiated, proliferative state. They are downregulated when differentiation is initiated. For placode-derived neurons, this involves a dose-dependent regulation of SoxB1 transcription factors. Mutations in SIX and EYA genes underlie several human syndromes whose phenotypes often include hearing loss.
KW - BMP
KW - Branchio-otic syndrome
KW - Branchio-otic-renal syndrome
KW - Eya genes
KW - FGF
KW - Pax genes
KW - Retinoic acid
KW - Six genes
KW - Wnt
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U2 - 10.1016/B978-0-12-405945-0.00019-3
DO - 10.1016/B978-0-12-405945-0.00019-3
M3 - Chapter
AN - SCOPUS:84922909093
SN - 9780124059450
SP - 331
EP - 356
BT - Principles of Developmental Genetics
PB - Elsevier Inc.
ER -