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FOXF2 is required for cochlear development in humans and mice.

Guney Bademci1, Clemer Abad1, Armagan Incesulu2

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A novel FOXF2 gene variant causes profound sensorineural hearing loss (SNHL) and cochlear anomalies. This discovery sheds light on the molecular mechanisms of human cochlear development and SNHL.

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Area of Science:

  • Genetics
  • Developmental Biology
  • Otolaryngology

Background:

  • The molecular underpinnings of human cochlear development are not well understood.
  • Sensorineural hearing loss (SNHL) is a common condition with diverse causes.
  • Cochlear malformations can lead to significant hearing impairment.

Purpose of the Study:

  • To investigate the genetic basis of SNHL associated with cochlear anomalies.
  • To identify novel genes involved in human cochlear development.
  • To elucidate the function of FOXF2 in cochlear formation.

Main Methods:

  • Whole-genome sequencing to identify genetic variants.
  • In vitro studies to assess protein stability.
  • Murine knockout models to study gene function in vivo.
  • Gene expression analysis in mouse cochleae.

Main Results:

  • A homozygous FOXF2 variant (c.325A>T, p.I109F) was identified in a patient with SNHL and cochlear malformation.
  • The identified FOXF2 variant reduces protein half-life.
  • Foxf2 knockout mice exhibit shortened, malformed cochleae and hair cell defects.
  • Expression of key developmental genes (Eya1, Pax3) is reduced in Foxf2 knockout mice.

Conclusions:

  • FOXF2 is crucial for normal cochlear development in both humans and mice.
  • FOXF2 dysfunction leads to SNHL and cochlear developmental anomalies.
  • This study identifies FOXF2 as a significant factor in auditory system development.