Epithelial-mesenchymal interactions are required for msx 1 and msx 2 gene expression in the developing murine molar tooth.

Epithelial-mesenchymal interactions are required for msx 1 and msx 2 gene expression in the developing murine molar tooth.
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发表时间:
1993-02
期刊:
影响因子:
4.6
通讯作者:
A. Jowett;S. Vainio;M. Ferguson;P. Sharpe;I. Thesleff
A. Jowett;S. Vainio;M. Ferguson;P. Sharpe;I. Thesleff
中科院分区:
生物学2区
文献类型:
--
作者:
A. Jowett;S. Vainio;M. Ferguson;P. Sharpe;I. Thesleff

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果蝇的msh样同源盒基因的重复可能与脊椎动物头部的进化有关。该基因的小鼠同源基因msx1和msx2在发育中的颅面复合体(包括鳃弓)中表达,特别是在上皮间充质器官发生区域(包括发育中的牙齿)中表达。通过使用E10 - E18小鼠胚胎的同慢性牙齿和非牙齿上皮和间质组织进行体外重组实验,我们发现牙齿中同源盒基因表达的维持依赖于组织相互作用。在同型重组中,牙型组织相互作用发生,导致两种基因的表达方式与体内发育过程中所见的相似。msx1仅在牙乳头和牙毛囊的间质中表达。msx2在牙上皮中表达,仅在牙乳头间质中表达。在异型重组中,牙上皮能够诱导非牙间质中msx1的表达,这种潜能在钟形期消失。在这些重组体中,msx2在芽期之前被推定的牙上皮诱导,但在芽期之后则不被诱导。牙间质中msx1和msx2的表达需要上皮的存在,直到钟状早期。然而,在牙齿发育的整个过程中,非牙齿的口腔上皮能够在牙间质中维持msx1的表达,而msx2的诱导则暂时受到限制,这表明与牙齿形成的诱导事件相关的特定上皮-间质相互作用调节了msx2的表达。msx1和msx2作为公认的转录因子,可能在牙齿形成过程中调控其他基因的表达。我们得出结论,颌骨间质中msx1的表达需要非特异性上皮信号,而msx2在上皮或间质中的表达需要特化牙细胞群之间的相互作用。
Duplication of the msh-like homeobox gene of Drosophila may be related to the evolution of the vertebrate head. The murine homologues of this gene, msx 1 and msx 2 are expressed in the developing craniofacial complex including the branchial arches, especially in regions of epithelial-mesenchymal organogenesis including the developing tooth. By performing in vitro recombination experiments using homochronic dental and non-dental epithelial and mesenchymal tissues from E10 to E18 mouse embryos, we have found that the maintenance of homeobox gene expression in the tooth is dependent upon tissue interactions. In homotypic recombinants, dental-type tissue interactions occur, leading to expression of both genes in a manner similar to that seen during in vivo development. msx 1 is expressed exclusively in mesenchyme, both in the dental papilla and follicle. msx 2 is expressed in the dental epithelium and only in the mesenchyme of the dental papilla. In heterotypic recombinants, the dental epithelium is able to induce msx 1 expression in non-dental mesenchyme, this potential being lost at the bell stage. In these recombinants msx 2 was induced by presumptive dental epithelium prior to the bud stage but not thereafter. The expression of msx 1 and msx 2 in dental mesenchyme requires the presence of epithelium until the early bell stage. However, whereas non-dental, oral epithelium is capable of maintaining expression of msx 1 in dental mesenchyme throughout tooth development, induction of msx 2 was temporally restricted suggesting regulation by a specific epithelial-mesenchymal interaction related to the inductive events of tooth formation. msx 1 and msx 2, as putative transcription factors, may play a role in regulating the expression of other genes during tooth formation. We conclude that expression of msx 1 in jaw mesenchyme requires a non-specific epithelial signal, whereas msx 2 expression in either epithelium or mesenchyme requires reciprocal interactions between specialized dental cell populations.