ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2014
Compensatory regulation of the size of the inner ear in response to excess induction of otic progenitors by fibroblast growth factor signaling.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Lipid-mediated reinforcement of FGF/MAPK signaling enables robust otic placode specification.bioRxiv : the preprint server for biology · 2026Article
- Craniosynostosis, inner ear, and renal anomalies in a child with complete loss ofJournal of medical genetics · 2023Article
- A gene network regulated by FGF signalling during ear development.Scientific reports · 2017Article
- Recovery of shape and size in a developing organ pair.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Article
- MEKK4 Signaling Regulates Sensory Cell Development and Function in the Mouse Inner Ear.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Cooperative and independent functions of FGF and Wnt signaling during early inner ear development.BMC developmental biology · 2015Article
- The Fibroblast Growth Factor signaling pathway.Wiley interdisciplinary reviews. Developmental biologyReview
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundThe otic placode comprises the progenitors of the inner ear and the neurons that convey hearing and balance information to the brain. Transplantation studies in birds and amphibians demonstrate that when the otic placode is morphologically visible as a thickened patch of ectoderm, it is first committed to an otic fate. Fibroblast growth factor (FGF) signaling initiates induction of the otic placode, and levels of FGF signaling are fine-tuned by the Sprouty family of antagonists of receptor tyrosine kinase signaling.
resultsHere, we examined the size of the otic placode and cup by combinatorial inactivation of the Sprouty1 and Sprouty2 genes. Interestingly, in a Sprouty gene dosage series, early enlargement of the otic placode was progressively restored to normal. Restoration of otic size was preceded by normal levels of FGF signaling, reduced cell proliferation and reduced cell death.
conclusionsOur study demonstrates that excess otic placode cells, which form in response to increased FGF signaling, are not maintained in mammals. This suggests that growth plasticity exists in the mammalian otic placode and cup, and that FGF signaling may not be sufficient to induce the genetic program that maintains otic fate.
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