Sprouty2 and Sprouty4 are essential for embryonic morphogenesis and regulation of FGF signaling

Koji Taniguchi, Toranoshin Ayada, Kenji Ichiyama, Ri ichiro Kohno, Yoshikazu Yonemitsu, Yasuhiro Minami, Akira Kikuchi, Yoshihiko Maehara, Akihiko Yoshimura

Research output: Contribution to journalArticle

83 Citations (Scopus)

Abstract

Sprouty genes encode cytoplasmic membrane-associated proteins that inhibit receptor tyrosine kinase signaling. Four orthologs of Drosophila Sprouty (dSpry) (Sprouty1-4) have been identified in mammals. Physiological function of Sprouty1 and Sprouty2 has been investigated using gene targeting approaches, however to date detailed examination of Sprouty4 knockout (KO) mice has not been reported. In this study, Sprouty4 KO mice were generated and characterized. Although a significant fraction of Sprouty4 KO mice died shortly after birth due to mandible defects, the remainder were viable and fertile. Growth retardation was observed for most Sprouty4-deficient mice, with nearly all Sprouty4 KO mice having polysyndactyly. ERK activation was sustained in Sprouty4 KO mouse embryonic fibroblasts (MEFs) in response to FGF, but not to EGF. Sprouty2 and Sprouty4 double KO (DKO) mice were embryonic lethal and showed severe defects in craniofacial, limb, and lung morphogenesis. These findings suggest both redundant and non-redundant functions for Sprouty2 and Sprouty4 on embryonic development and FGF signaling.

Original languageEnglish
Pages (from-to)896-902
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume352
Issue number4
DOIs
Publication statusPublished - Jan 26 2007

    Fingerprint

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this