Fish scale development: Hair today, teeth and scales yesterday?

@article{Sharpe2001FishSD,
  title={Fish scale development: Hair today, teeth and scales yesterday?},
  author={Paul T. Sharpe},
  journal={Current Biology},
  year={2001},
  volume={11},
  pages={R751-R752}
}
  • P. Sharpe
  • Published 2001
  • Biology, Medicine
  • Current Biology
A group of genes in the tumour necrosis factor signalling pathway are mutated in humans and mice with ectodermal dysplasias--a failure of hair and tooth development. A mutation has now been identified in one of these genes, ectodysplasin-A receptor, in the teleost fish Medaka, that results in a failure of scale formation. 
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References

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The medaka rs-3 locus required for scale development encodes ectodysplasin-A receptor
TLDR
It is demonstrated that the rs-3 locus encodes ectodysplasin-A receptor (EDAR), which is required for the initiation of hair development in mammals, and a novel transposon inserted in the first intron of EDAR, which causes aberrant splicing is identified. Expand
Splitting Hairs Dissecting Roles of Signaling Systems in Epidermal Development
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Experiments suggest that placodes induced by activators ond, cells in the placode differentiate into several types like FGF are surrounded by cells prevented from adopt- that grow into all the structures of the mature hair or ing a placode fate by the overriding activity of inhibitors feather. Expand
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The developing tooth has proven to be an excellent model in studies of the molecular basis of patterning and morphogenesis of organs and it can be expected that continuing studies will rapidly increase the understanding of these mechanisms. Expand
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The positional cloning of the gene mutated in EDA is described, which encode a predicted 135–residue transmembrane protein that may belong to a novel class with a role in epithelial–mesenchymal signalling. Expand
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TLDR
A candidate cDNA is identified for the mouse Tabby gene (Ta), which, based on phenotype and syntenic mapping, is postulated to represent the analogous murine disorder XLHED, and the predicted extracellular collagenous domain of this membrane protein may play a key role in epithelial-mesenchymal interactions. Expand
The Tabby phenotype is caused by mutation in a mouse homologue of the EDA gene that reveals novel mouse and human exons and encodes a protein (ectodysplasin-A) with collagenous domains.
TLDR
The Ta gene is cloned and it is found to be homologous to the EDA gene, which encodes a 391-residue transmembrane protein, ectodysplasin-A, containing 19 Gly-Xaa-Yaa repeats. Expand
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A complete splicing map of the EDA gene is built up and the longest and what most probably represents the full-length EDA transcript, EDA-A is characterized, which encodes a 391 amino acid transmembrane protein with a short collagenous domain, (Gly-X-Y)19, and is highly homologous to the protein mutated in Tabby mice. Expand
Mutations in the human homologue of mouse dl cause autosomal recessive and dominant hypohidrotic ectodermal dysplasia
X-linked hypohidrotic ectodermal dysplasia results in abnormal morphogenesis of teeth, hair and eccrine sweat glands. The gene (ED1) responsible for the disorder has been identified, as well as theExpand
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The evolutionary links that exist between odontodes and organs that are phylogenetically related to them (teeth and scales) suggest the use of comparative approaches to study these structures, and the current state of knowledge on developmental mechanisms involved in non-mammalian odontogenesis is reviewed. Expand
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