Analysis of FGF-Dependent and FGF-Independent Pathways in Otic Placode Induction
Author
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Yang, Lu
Author
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O’Neill, Paul
es_CL
Author
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Martin, Kareen
es_CL
Author
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Maass Oñate, Juan
es_CL
Author
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Vassilev, Vassil
es_CL
Author
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Ladher, Raj
es_CL
Author
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Groves, Andrew K.
es_CL
Admission date
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2014-01-29T20:03:13Z
Available date
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2014-01-29T20:03:13Z
Publication date
dc.date.issued
2013-01-23
Cita de ítem
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PLoS ONE 8(1): e55011
en_US
Identifier
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doi:10.1371/journal.pone.0055011
Identifier
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https://repositorio.uchile.cl/handle/2250/129218
General note
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Artículo de publicación ISI
en_US
Abstract
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The inner ear develops from a patch of thickened cranial ectoderm adjacent to the hindbrain called the otic placode. Studies in a number of vertebrate species suggest that the initial steps in induction of the otic placode are regulated by members of the Fibroblast Growth Factor (FGF) family, and that inhibition of FGF signaling can prevent otic placode formation. To better understand the genetic pathways activated by FGF signaling during otic placode induction, we performed microarray experiments to estimate the proportion of chicken otic placode genes that can be up-regulated by the FGF pathway in a simple culture model of otic placode induction. Surprisingly, we find that FGF is only sufficient to induce about 15% of chick otic placode-specific genes in our experimental system. However, pharmacological blockade of the FGF pathway in cultured chick embryos showed that although FGF signaling was not sufficient to induce the majority of otic placode-specific genes, it was still necessary for their expression in vivo. These inhibitor experiments further suggest that the early steps in otic placode induction regulated by FGF signaling occur through the MAP kinase pathway. Although our work suggests that FGF signaling is necessary for otic placode induction, it demonstrates that other unidentified signaling pathways are required to co-operate with FGF signaling to induce the full otic placode program.
en_US
Patrocinador
dc.description.sponsorship
National Institutes of Health (NIH) DC004675 (A.K.G.), NIH DC008692 (K.M.), RIKEN FPR fellowship (P.O.), RIKEN intramural
funding (P.O. and R.L.) and a fellowship from MECESUP (UCH0603, Ministerio de Educacio´ n, Gobierno de Chile, J.C.M.).