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Sprouty1 and Sprouty2 limit both the size of the otic placode and hindbrain Wnt8a by antagonizing FGF signaling

Amanda A Mahoney Rogers1, Jian Zhang, Katherine Shim

  • 1Department of Pediatrics, Children's Research Institute, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA.

Developmental Biology
|March 3, 2011
PubMed

Insights

SPRY1 and SPRY2 proteins regulate inner ear development. Loss of these proteins causes the otic placode to enlarge by recruiting adjacent cells, a process linked to Wnt signaling and rescued by modulating Fibroblast Growth Factor 10.

Area of Science:

  • Developmental biology
  • Molecular and cellular biology
  • Genetics

Background:

  • Fibroblast Growth Factor (FGF) and Wnt signaling pathways are crucial for inner ear (otic placode) development.
  • SPRY proteins are known inhibitors of FGF signaling, but their precise role in otic placode formation is unclear.

Purpose of the Study:

  • To investigate the role of SPRY1 and SPRY2 in the formation and size regulation of the otic placode.
  • To elucidate the molecular mechanisms by which SPRY proteins influence otic placode development and cell recruitment.

Main Methods:

  • Generation and analysis of compound Spry1⁻/⁻; Spry2⁻/⁻ mutant mouse embryos.
  • Assessment of otic placode size and cell fate.
  • Analysis of Wnt8a expression patterns.
  • Genetic manipulation by reducing Fgf10 gene dosage.

Main Results:

  • Spry1⁻/⁻; Spry2⁻/⁻ embryos exhibit an enlarged otic placode.
  • The enlarged otic placode results from the recruitment of cranial epidermis cells.
  • Otic placode enlargement and Wnt8a domain expansion in mutants are rescued by reducing Fgf10 dosage.

Conclusions:

  • SPRY proteins act as critical regulators of otic placode size by controlling cell recruitment.
  • A FGF-responsive window exists for continuous cell recruitment into the otic domain.
  • SPRY proteins modulate the size of Wnt signaling centers during inner ear development.

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