FGFs control the patterning of the inner ear but are not able to induce the full ear program

Mech Dev. 2001 Dec;109(2):303-13. doi: 10.1016/s0925-4773(01)00550-0.

Abstract

FGF2 or FGF8 applied ectopically, close to the developing otic placode enhances transcription of a subset of ear marker genes such as Nkx5-1, SOHo1 and Pax2. Other ear expressed genes (Dlx5 and BMP4) are not up-regulated by FGFs. Ectopic FGFs lead to an increase in size of the vestibulo-cochlear ganglion. This phenotypic change is due to an increased recruitment of epithelial cells to the neuronal fate rather than to an enhanced proliferation. We also observed an induction of additional, vesicle-like structures upon ectopic FGF treatment, but this induction never led to enrolment of a full ear program. We further demonstrate that FGF8 is expressed in two separate, short waves, first at the otic placode stage and later at the vesicle stage. Both activities correspond to critical morphogenetic events in ear development. We propose that FGF8 is an important regulator of otocyst patterning.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cell Division
  • Cell Lineage
  • Chick Embryo
  • Cochlea / innervation
  • DNA, Complementary / metabolism
  • Ear, Inner / embryology*
  • Ear, Inner / physiology*
  • Fibroblast Growth Factor 2 / metabolism*
  • Fibroblast Growth Factor 2 / physiology
  • Fibroblast Growth Factor 8
  • Fibroblast Growth Factors / metabolism*
  • Fibroblast Growth Factors / physiology*
  • Ganglia / physiology
  • In Situ Hybridization
  • Models, Statistical
  • Phenotype
  • Protein Structure, Tertiary
  • Software
  • Time Factors

Substances

  • DNA, Complementary
  • Fibroblast Growth Factor 2
  • Fibroblast Growth Factor 8
  • Fibroblast Growth Factors