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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Tissue morphogenesis and vascular stability require the Frem2 protein, product of the mouse myelencephalic blebs gene
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Tissue morphogenesis and vascular stability require the Frem2 protein, product of the mouse myelencephalic blebs gene

机译：组织形态发生和血管稳定性需要Frem2蛋白，Frem2蛋白是小鼠骨髓性脑泡基因的产物

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摘要

Adhesive properties of cells undergoing morphogenetic rearrangements can be regulated either at the cellular level or by altering the environment in which rearrangements occur. Here, we describe the identification of a mutation (my(F11)) in the mouse extracellular matrix component Frem2, and provide evidence that suggests Frem2 expression creates an environment conducive to morphogenetic events. Loss of Frem2 function results in defects in developmental events associated with morphogenetic rearrangements of the vasculature and of tissues arising from all germ layers. The Frem2 transcript is restricted both spatially and temporally and appears in advance of cell rearrangement events. Thus, expression of Frem2 may dynamically alter the extracellular matrix to provide a substrate for cell migration and rearrangements during embryogenesis.
机译：可以在细胞水平或通过改变发生重排的环境来调节经历形态发生重排的细胞的粘附特性。在这里，我们描述了小鼠细胞外基质成分Frem2中的突变（my（F11））的鉴定，并提供了表明Frem2表达创造有利于形态发生事件的环境的证据。 Frem2功能的丧失导致与所有细菌层引起的血管和组织形态发生重排相关的发育事件缺陷。 Frem2转录本在空间和时间上都受到限制，并在细胞重排事件之前出现。因此，Frem2的表达可以动态地改变细胞外基质，为胚胎发生过程中的细胞迁移和重排提供底物。

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