MSX1 DEFICIENT MICE EXHIBIT CLEFT-PALATE AND ABNORMALITIES OF CRANIOFACIAL AND TOOTH DEVELOPMENT
MSX1 DEFICIENT MICE EXHIBIT CLEFT-PALATE AND ABNORMALITIES OF CRANIOFACIAL AND TOOTH DEVELOPMENT
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DOI：
10.1038/ng0494-348
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发表时间：
1994-04-01
期刊：
影响因子：
30.8
通讯作者：
MAAS, R
中科院分区：
文献类型：
--
作者：
SATOKATA, I;MAAS, R
Msx 1同源异型盒基因在脊椎动物胚胎发生过程中的上皮-间充质相互作用的不同位点表达，并参与组织层之间的信号传导过程。为了确定其缺陷的表型后果，我们制备了缺乏Msx 1功能的小鼠。所有Msx 1纯合子均表现为继发腭裂、牙槽骨缺失和牙齿发育障碍。这些小鼠还表现出鼻骨、额骨和顶骨以及中耳锤骨的异常。因此，Msx 1在颅面骨和牙齿发育过程中介导上皮-间充质相互作用方面发挥着关键作用。Msx 1-/Msx 1-表型与人类腭裂相似，并为腭裂和缺牙提供了一个已知缺陷基因的遗传模型。
The Msx1 homeobox gene is expressed at diverse sites of epithelial-mesenchymal interaction during vertebrate embryogenesis, and has been implicated in signalling processes between tissue layers. To determine the phenotypic consequences of its deficiency, we prepared mice lacking Msx1 function. All Msx1-homczygotes manifest a cleft secondary palate, a deficiency of alveolar mandible and maxilla and a failure of tooth development. These mice also exhibit abnormalities of the nasal, frontal and parietal bones, and of the malleus in the middle ear. Msx1 thus has a critical role in mediating epithelial-mesenchymal interactions during craniofacial bone and tooth development. The Msx1-/Msx1- phenotype is similar to human cleft palate, and provides a genetic model for cleft palate and oligodontia in which the defective gene is known.