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Eda 通路突变体中小唾液腺的缺陷和挽救。

Defects and rescue of the minor salivary glands in Eda pathway mutants.

机构信息

Department of Craniofacial Development, King's College London Dental Institute, London SE1 9RT, UK.

出版信息

Dev Biol. 2011 Jan 15;349(2):137-46. doi: 10.1016/j.ydbio.2010.10.012. Epub 2010 Oct 20.

Abstract

Despite their importance to oral health, the mechanisms of minor salivary gland (SG) development are largely unexplored. Here we present in vivo and in vitro analyses of developing minor SGs in wild type and mutant mice. Eda, Shh and Fgf signalling pathway genes are expressed in these glands from an early stage of development. Developing minor SGs are absent in Eda pathway mutant embryos, and these mice exhibit a dysplastic circumvallate papilla with disrupted Shh expression. Supplementation of Eda pathway mutant minor SG explants with recombinant EDA rescues minor SG induction. Supplementation with Fgf8 or Shh, previously reported targets of Eda signalling, leads to induction of gland like structures in a few cases, but these fail to develop into minor SGs.

摘要

尽管它们对口腔健康很重要,但小唾液腺(SG)发育的机制在很大程度上仍未得到探索。在这里,我们对野生型和突变型小鼠的发育中小唾液腺进行了体内和体外分析。Eda、Shh 和 Fgf 信号通路基因在这些腺体的早期发育阶段表达。Eda 通路突变体胚胎中缺少发育中的小唾液腺,这些小鼠表现出环状乳头发育不良,Shh 表达中断。用重组 EDA 补充 Eda 通路突变体小唾液腺外植体可挽救小唾液腺的诱导。先前报道的 Eda 信号的靶基因 Fgf8 或 Shh 的补充可在少数情况下诱导类似腺体的结构,但这些结构不能发育成小唾液腺。

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