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A requirement for Fgfr2 in middle ear development.

Diana Rigueur1,2, Ryan R Roberts1,2, Lauren Bobzin1,2

  • 1Center for Craniofacial Molecular Biology, Ostrow School of Dentistry, University of Southern California, Los Angeles, California.

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|September 26, 2018
PubMed
Summary
This summary is machine-generated.

Fibroblast growth factor receptor 2 (FGFR2) loss-of-function mutations cause LADD syndrome. This study reveals FGFR2 is crucial for middle ear skeletal development, identifying potential causes of conductive hearing loss in LADD syndrome.

Keywords:
Fgfr2auditory ossiclescraniofacial developmentjoint developmentskeletal development

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Area of Science:

  • Developmental Biology
  • Genetics
  • Otolaryngology

Background:

  • The mammalian middle ear's skeletal structure is vital for sound conduction.
  • Gene mutations affecting middle ear skeletal development can lead to auditory impairment.
  • Fibroblast growth factor receptor 2 (FGFR2) mutations cause skeletal disorders, including conductive hearing loss.

Purpose of the Study:

  • To investigate the role of FGFR2 in the development of the middle ear skeleton.
  • To understand the causes of conductive hearing loss in lacrimo-auriculo-dento-digital (LADD) syndrome, a loss-of-function FGFR2 disorder.

Main Methods:

  • Examined the middle ear skeleton in mice with conditional loss of Fgfr2.
  • Analyzed auditory function, skeletal morphology, and gene expression patterns.

Main Results:

  • FGFR2 loss in mice correlated with reduced auditory function, auditory bulla hypoplasia, and ectopic bone growth.
  • Ectopic bone near the incudomalleal joint originated from Scx-expressing cells.
  • Decreased expression of the joint progenitor marker Gdf5 was observed.

Conclusions:

  • FGFR2 plays a significant role in the development of middle ear skeletal tissues.
  • Abnormal skeletal development, including ectopic bone formation, may cause conductive hearing loss in LADD syndrome.