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Context-specific requirements for Fgfr1 signaling through Frs2 and Frs3 during mouse development

Renée V Hoch1, Philippe Soriano

  • 1Program in Developmental Biology, Division of Basic Sciences, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue North, Seattle, WA 98109, USA.

Development (Cambridge, England)
|January 20, 2006
PubMed

Insights

Fibroblast growth factor receptor 1 (Fgfr1) signaling is essential for embryonic development. Some Fgfr1 functions rely on Frs2/3-dependent pathways, while others utilize Frs-independent signaling.

Area of Science:

  • Developmental biology
  • Molecular signaling
  • Genetics

Background:

  • Fibroblast growth factor receptor 1 (Fgfr1) has critical roles in embryonic development.
  • Fgf receptor-specific substrates (Frs2, Frs3) are known mediators of Fgfr1 signaling to MAPK and PI3K pathways.

Purpose of the Study:

  • To investigate the in vivo signaling mechanisms of Fgfr1 during embryonic development.
  • To determine the necessity of Frs2/3 binding for Fgfr1 function.

Main Methods:

  • Generation of Fgfr1(Delta)Frs/DeltaFrs mutant mice lacking the Frs2/3-binding site on Fgfr1.
  • Analysis of embryonic development, including neural tube closure, tail bud, and pharyngeal arch formation.
  • Assessment of Fgfr1 signaling via MAPK pathway activation.

Main Results:

  • Fgfr1(Delta)Frs/DeltaFrs embryos exhibit embryonic lethality during late embryogenesis.
  • Mutant embryos show defects in neural tube closure, tail bud, and pharyngeal arch development.
  • The mutant receptor retains Fgfr1 functions during gastrulation and somitogenesis, and supports normal MAPK signaling.

Conclusions:

  • Fgfr1 utilizes distinct signal transduction pathways in different developmental stages.
  • Essential embryonic functions of Fgfr1 can be mediated independently of Frs2/3 binding.
  • This highlights the complexity of Fgfr1 signaling in vivo.

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