The mouse snail gene encodes a key regulator of the epithelial-mesenchymal transition
The mouse snail gene encodes a key regulator of the epithelial-mesenchymal transition
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DOI：
10.1128/mcb.21.23.8184-8188.2001
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发表时间：
2001-12-01
影响因子：
5.3
通讯作者：
Gridley, T
中科院分区：
文献类型：
--
作者：
Carver, EA;Jiang, RL;Gridley, T
Snail家族基因编码DNA结合锌指蛋白，作为转录抑制因子。缺乏Snail（Sna）基因的小鼠胚胎在中胚层的形成中表现出缺陷。在Sna（-/-）突变体胚胎中，中胚层形成，中胚层标记基因被诱导，但突变的中胚层形态异常。陷窝形成于突变胚胎的中胚层内，排列在这些陷窝内的细胞保留上皮细胞的特征。这些细胞类似于柱状上皮，具有顶-基底极性，沿顶面沿着有微绒毛，细胞间电子致密的粘附连接类似于粘附连接。在Sna（-/-）胚胎的中胚层中保留了E-钙粘蛋白的表达。这些缺陷是惊人的相似，在蜗牛缺陷果蝇胚胎中观察到的原肠胚形成缺陷，这表明蜗牛家族蛋白的E-钙粘蛋白转录的抑制机制可能已经存在于节肢动物和哺乳动物谱系的后生动物祖先。
Snail family genes encode DNA binding zinc finger proteins that act as transcriptional repressors. Mouse embryos deficient for the Snail (Sna) gene exhibit defects in the formation of the mesoderm germ layer. In Sna(-/-) mutant embryos, a mesoderm layer forms and mesodermal marker genes are induced but the mutant mesoderm is morphologically abnormal. Lacunae form within the mesoderm layer of the mutant embryos, and cells lining these lacunae retain epithelial characteristics. These cells resemble a columnar epithelium and have apical-basal polarity, with microvilli along the apical surface and intercellular electron-dense adhesive junctions that resemble adherens junctions. E-cadherin expression is retained in the mesoderm of the Sna(-/-) embryos. These defects are strikingly similar to the gastrulation defects observed in snail-deficient Drosophila embryos, suggesting that the mechanism of repression of E-cadherin transcription by Snail family proteins may have been present in the metazoan ancestor of the arthropod and mammalian lineages.