Ectodysplasin, Edar and TNFRSF19 are expressed in complementary and overlapping patterns during mouse embryogenesis
Section snippets
Results and discussion
Ectodysplasin (Eda) and its receptor Edar are the first members of the tumor necrosis factor (TNF) and TNF receptor superfamilies, respectively, that have been implicated in the regulation of embryonic morphogenesis. Lack of ectodysplasin or Edar results in ectodermal dysplasia, i.e. deficient development of several ectodermal appendages, including teeth and hair. Mutations in the human and mouse Eda genes cause the X-linked hypo- or anhidrotic ectodermal dysplasia syndrome (HED or EDA) and the
Materials and methods
Radioactive in situ hybridisation on paraffin-embedded tissue sections was performed according to standard protocols (Wilkinson and Green, 1990). In situ hybridisation on whole-mount tissues was performed either manually (Kettunen and Thesleff, 1998) or with an InsituPro robot (Intavis, Germany). Approximately 100 μm thick sections were cut with a vibratome from whole-mount in situ hybridisation tissues. Eda probe has been previously published (Laurikkala et al., 2001). Edar and TNFRSF19 probes
Acknowledgements
We thank Merja Mäkinen, Ludmila Rasskozova, Riikka Santalahti, and Sari Suomi for excellent technical assistance. This work has been supported by the Academy of Finland, the Sigrid Juselius Foundation, and the Emil Aaltonen Foundation.
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