Expression and function of FGF10 in mammalian inner ear development

Sarah Pauley, Tracy J. Wright, Ulla Pirvola, David Ornitz, Kirk Beisel, Bernd Fritzsch

Research output: Contribution to journalArticle

162 Citations (Scopus)

Abstract

We have investigated the expression of FGF10 during ear development and the effect of an FGF10 null mutation on ear development. Our in situ hybridization data reveal expression of FGF10 in all three canal crista sensory epithelia and the cochlea anlage as well as all sensory neurons at embryonic day 11.5 (E11.5). Older embryos (E18.5) displayed strong graded expression in all sensory epithelia. FGF10 null mutants show complete agenesis of the posterior canal crista and the posterior canal. The posterior canal sensory neurons form initially and project rather normally by E11.5, but they disappear within 2 days. FGF10 null mutants have no posterior canal system at E18.5. In addition, these mutants have deformations of the anterior and horizontal cristae, reduced formation of the anterior and horizontal canals, as well as altered position of the remaining sensory epithelia with respect to the utricle. Hair cells form but some have defects in their cilia formation. No defects were detected in the organ of Corti at the cellular level. Together these data suggest that FGF10 plays a major role in ear morphogenesis. Most of these data are consistent with earlier findings on a null mutation in FGFR2b, one of FGF10's main receptors.

Original languageEnglish
Pages (from-to)203-215
Number of pages13
JournalDevelopmental Dynamics
Volume227
Issue number2
DOIs
StatePublished - Jun 1 2003

Fingerprint

Inner Ear
Ear
Epithelium
Sensory Receptor Cells
Receptor, Fibroblast Growth Factor, Type 2
Saccule and Utricle
Organ of Corti
Mutation
Cilia
Cochlea
Morphogenesis
In Situ Hybridization
Embryonic Structures

All Science Journal Classification (ASJC) codes

  • Developmental Biology
  • Cell Biology

Cite this

Pauley, S., Wright, T. J., Pirvola, U., Ornitz, D., Beisel, K., & Fritzsch, B. (2003). Expression and function of FGF10 in mammalian inner ear development. Developmental Dynamics, 227(2), 203-215. https://doi.org/10.1002/dvdy.10297

Expression and function of FGF10 in mammalian inner ear development. / Pauley, Sarah; Wright, Tracy J.; Pirvola, Ulla; Ornitz, David; Beisel, Kirk; Fritzsch, Bernd.

In: Developmental Dynamics, Vol. 227, No. 2, 01.06.2003, p. 203-215.

Research output: Contribution to journalArticle

Pauley, S, Wright, TJ, Pirvola, U, Ornitz, D, Beisel, K & Fritzsch, B 2003, 'Expression and function of FGF10 in mammalian inner ear development', Developmental Dynamics, vol. 227, no. 2, pp. 203-215. https://doi.org/10.1002/dvdy.10297
Pauley, Sarah ; Wright, Tracy J. ; Pirvola, Ulla ; Ornitz, David ; Beisel, Kirk ; Fritzsch, Bernd. / Expression and function of FGF10 in mammalian inner ear development. In: Developmental Dynamics. 2003 ; Vol. 227, No. 2. pp. 203-215.
@article{a4acefb3e8954a6f85c89548b04172da,
title = "Expression and function of FGF10 in mammalian inner ear development",
abstract = "We have investigated the expression of FGF10 during ear development and the effect of an FGF10 null mutation on ear development. Our in situ hybridization data reveal expression of FGF10 in all three canal crista sensory epithelia and the cochlea anlage as well as all sensory neurons at embryonic day 11.5 (E11.5). Older embryos (E18.5) displayed strong graded expression in all sensory epithelia. FGF10 null mutants show complete agenesis of the posterior canal crista and the posterior canal. The posterior canal sensory neurons form initially and project rather normally by E11.5, but they disappear within 2 days. FGF10 null mutants have no posterior canal system at E18.5. In addition, these mutants have deformations of the anterior and horizontal cristae, reduced formation of the anterior and horizontal canals, as well as altered position of the remaining sensory epithelia with respect to the utricle. Hair cells form but some have defects in their cilia formation. No defects were detected in the organ of Corti at the cellular level. Together these data suggest that FGF10 plays a major role in ear morphogenesis. Most of these data are consistent with earlier findings on a null mutation in FGFR2b, one of FGF10's main receptors.",
author = "Sarah Pauley and Wright, {Tracy J.} and Ulla Pirvola and David Ornitz and Kirk Beisel and Bernd Fritzsch",
year = "2003",
month = "6",
day = "1",
doi = "10.1002/dvdy.10297",
language = "English",
volume = "227",
pages = "203--215",
journal = "Developmental Dynamics",
issn = "1058-8388",
publisher = "Wiley-Liss Inc.",
number = "2",

}

TY - JOUR

T1 - Expression and function of FGF10 in mammalian inner ear development

AU - Pauley, Sarah

AU - Wright, Tracy J.

AU - Pirvola, Ulla

AU - Ornitz, David

AU - Beisel, Kirk

AU - Fritzsch, Bernd

PY - 2003/6/1

Y1 - 2003/6/1

N2 - We have investigated the expression of FGF10 during ear development and the effect of an FGF10 null mutation on ear development. Our in situ hybridization data reveal expression of FGF10 in all three canal crista sensory epithelia and the cochlea anlage as well as all sensory neurons at embryonic day 11.5 (E11.5). Older embryos (E18.5) displayed strong graded expression in all sensory epithelia. FGF10 null mutants show complete agenesis of the posterior canal crista and the posterior canal. The posterior canal sensory neurons form initially and project rather normally by E11.5, but they disappear within 2 days. FGF10 null mutants have no posterior canal system at E18.5. In addition, these mutants have deformations of the anterior and horizontal cristae, reduced formation of the anterior and horizontal canals, as well as altered position of the remaining sensory epithelia with respect to the utricle. Hair cells form but some have defects in their cilia formation. No defects were detected in the organ of Corti at the cellular level. Together these data suggest that FGF10 plays a major role in ear morphogenesis. Most of these data are consistent with earlier findings on a null mutation in FGFR2b, one of FGF10's main receptors.

AB - We have investigated the expression of FGF10 during ear development and the effect of an FGF10 null mutation on ear development. Our in situ hybridization data reveal expression of FGF10 in all three canal crista sensory epithelia and the cochlea anlage as well as all sensory neurons at embryonic day 11.5 (E11.5). Older embryos (E18.5) displayed strong graded expression in all sensory epithelia. FGF10 null mutants show complete agenesis of the posterior canal crista and the posterior canal. The posterior canal sensory neurons form initially and project rather normally by E11.5, but they disappear within 2 days. FGF10 null mutants have no posterior canal system at E18.5. In addition, these mutants have deformations of the anterior and horizontal cristae, reduced formation of the anterior and horizontal canals, as well as altered position of the remaining sensory epithelia with respect to the utricle. Hair cells form but some have defects in their cilia formation. No defects were detected in the organ of Corti at the cellular level. Together these data suggest that FGF10 plays a major role in ear morphogenesis. Most of these data are consistent with earlier findings on a null mutation in FGFR2b, one of FGF10's main receptors.

UR - http://www.scopus.com/inward/record.url?scp=0037945196&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037945196&partnerID=8YFLogxK

U2 - 10.1002/dvdy.10297

DO - 10.1002/dvdy.10297

M3 - Article

VL - 227

SP - 203

EP - 215

JO - Developmental Dynamics

JF - Developmental Dynamics

SN - 1058-8388

IS - 2

ER -