Expression of ptc and gli genes in talpid3 suggests bifurcation in Shh pathway
| Autor: | I. R. Paton, C. Tickle, Philip W. Ingham, Katharine E. Lewis, K. E. Robertson, D. R. Morrice, G. Drossopoulou, D. W. Burt |
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| Rok vydání: | 1999 |
| Předmět: |
Patched
Patched Receptors Receptors Steroid animal structures Limb Buds Bone Morphogenetic Protein 2 Receptors Cell Surface Chick Embryo Biology Polymerase Chain Reaction Zinc Finger Protein GLI1 Receptors G-Protein-Coupled Limb bud GLI1 Transforming Growth Factor beta GLI3 Animals Hedgehog Proteins Sonic hedgehog Molecular Biology Hedgehog In Situ Hybridization Polymorphism Single-Stranded Conformational Regulation of gene expression Genetics Oncogene Proteins Chromosome Mapping Gene Expression Regulation Developmental Membrane Proteins Proteins Cell biology DNA-Binding Proteins COUP Transcription Factors Phenotype embryonic structures Bone Morphogenetic Proteins Mutation Tissue Transplantation biology.protein Trans-Activators Genes Lethal Smoothened Developmental Biology Signal Transduction Transcription Factors |
| Zdroj: | Development (Cambridge, England). 126(11) |
| ISSN: | 0950-1991 |
| Popis: | talpid 3 is an embryonic-lethal chicken mutation in a molecularly un-characterised autosomal gene. The recessive, pleiotropic phenotype includes polydactylous limbs with morphologically similar digits. Previous analysis established that hox-D and bmp genes, that are normally expressed posteriorly in the limb bud in response to a localised, posterior source of Sonic Hedgehog (Shh) are expressed symmetrically across the entire anteroposterior axis in talpid3 limb buds. In contrast, Shh expression itself is unaffected. Here we examine expression of patched (ptc), which encodes a component of the Shh receptor, and is probably itself a direct target of Shh signalling, to establish whether talpid3 acts in the Shh pathway. We find that ptc expression is significantly reduced in talpid3 embryos. We also demonstrate that talpid3 function is not required for Shh signal production but is required for normal response to Shh signals, implicating talpid3 in transduction of Shh signals in responding cells. Our analysis of expression of putative components of the Shh pathway, gli1, gli3 and coupTFII shows that genes regulated by Shh are either ectopically expressed or no longer responsive to Shh signals in talpid3 limbs, suggesting possible bifurcation in the Shh pathway. We also describe genetic mapping of gli1, ptc, shh and smoothened in chickens and confirm by co-segregation analysis that none of these genes correspond to talpid3. |
| Databáze: | OpenAIRE |
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