Control of murine kidney development by sonic hedgehog and its GLI effectors.
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.
Gill
Paul S
PS
Program in Developmental Biology, The Hospital for Sick Children, Toronto, Canada.
Rosenblum
Norman D
ND
D000818:Animals; D018507:Gene Expression Regulation, Developmental; D053823:Hedgehog Proteins / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D007668:Kidney / Q000196:embryology* / Q000378:metabolism*; D051741:Kruppel-Like Transcription Factors / Q000235:genetics / Q000378:metabolism*; D051379:Mice; D011485:Protein Binding; D015398:Signal Transduction; D000071676:Zinc Finger Protein GLI1
C498520:Gli1 protein, mouse; D053823:Hedgehog Proteins; D051741:Kruppel-Like Transcription Factors; C465570:Shh protein, mouse; D000071676:Zinc Finger Protein GLI1