Control of murine kidney development by sonic hedgehog and its GLI effectors

Cell Cycle. 2006 Jul;5(13):1426-30. doi: 10.4161/cc.5.13.2928. Epub 2006 Jul 1.


Sonic hedgehog (SHH) controls cell differentiation and morphogenesis in many tissues and species. The mammalian kidney is a paradigm for studying epithelial-mesenchymal interactions and growth factor signaling during embryogenesis. Here, we review our recent findings demonstrating that SHH is required for normal murine kidney development. During renal morphogenesis, SHH controls a hierarchy of genes including renal patterning genes, cell cycle modulators, and GLI family members. Our investigation of GLI protein processing and binding of GLI activators and repressor to SHH target genes provide insight into the molecular mechanisms by which SHH and its GLI family of effectors control renal embryogenesis. Further, we highlight the roles of BMP, WNT and FGF signaling during renal development and discuss possible interactions of these pathways with SHH signaling.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Gene Expression Regulation, Developmental
  • Hedgehog Proteins / genetics
  • Hedgehog Proteins / metabolism*
  • Humans
  • Kidney / embryology*
  • Kidney / metabolism*
  • Kruppel-Like Transcription Factors / genetics
  • Kruppel-Like Transcription Factors / metabolism*
  • Mice
  • Protein Binding
  • Signal Transduction
  • Zinc Finger Protein GLI1


  • Gli1 protein, mouse
  • Hedgehog Proteins
  • Kruppel-Like Transcription Factors
  • Shh protein, mouse
  • Zinc Finger Protein GLI1