作者: A.S Tucker , D.J Headon , J.-M Courtney , P Overbeek , P.T Sharpe
DOI: 10.1016/J.YDBIO.2003.12.019
关键词:
摘要: Mutations in members of the ectodysplasin (TNF-related) signalling pathway, EDA, EDAR, and EDARADD mice humans produce an ectodermal dysplasia phenotype that includes missing teeth smaller with reduced cusps. Using keratin 14 promoter to target expression activated form Edar transgenic mice, we show this transgene is able rescue tooth Tabby (Eda) Sleek (Edar) mutant mice. High levels wild-type result molar extra cusps, some cases supernumerary teeth, opposite phenotype. The level activation thus determines cusp number during development.