Tooth Patterning and enamel formation can be manipulated by misexpression of TNF receptor Edar
Tooth Patterning and enamel formation can be manipulated by misexpression of TNF receptor Edar
复制标题
DOI：
10.1002/dvdy.20138
复制
发表时间：
2004-10-01
影响因子：
2.5
通讯作者：
Thesleff, I
中科院分区：
文献类型：
--
作者：
Pispa, J;Mustonen, T;Thesleff, I
肿瘤坏死因子受体 Edar 发出的信号是外胚层器官发育所必需的。 Edar 或同一信号通路的其他分子的突变会导致人类和小鼠的外胚层发育不良。在这些疾病中，牙齿缺失或畸形，毛发和一些腺体发育不良。在牙齿和毛发发育过程中，Edar 表达会形成外胚层基板和信号中心的模式。这种定位被认为是器官发生所必需的。我们使用角蛋白 14 启动子在整个外胚层中表达 Edar，并表明这种错误表达会破坏牙齿图案和分化。牙齿形状和牙尖数量受到不同的影响，具体取决于转基因表达的量。此外，牙釉质的形成存在剂量依赖性缺陷。我们推测牙齿图案缺陷是由信号中心外的异位 Edar 活动引起的。 (C) 2004 Wiley-Liss, Inc.
Signaling by Edar, a tumor necrosis factor receptor, is required for the development of ectodermal organs. Mutations in Edar or other molecules of the same signaling pathway cause ectodermal dysplasias in humans and mice. In these diseases, teeth are missing or malformed, and the development of hairs and several glands is hypoplastic. During tooth and hair development, Edar expression becomes patterned to ectodermal placodes and signaling centers. This localization has been suggested to be required for organogenesis. We have expressed Edar throughout the ectoderm using the keratin 14 promoter and show that this misexpression disrupts tooth patterning and differentiation. Tooth shape and cusp number are differentially affected, depending on the amount of transgene expression. In addition, tooth enamel formation is defective in a dose-dependent manner. We speculate that the tooth patterning defects are caused by ectopic Edar activity outside the signaling centers. (C) 2004 Wiley-Liss, Inc.