Antisense targeting of engrailed-1 causes abnormal axis formation in mouse embryos.
Antisense targeting of engrailed-1 causes abnormal axis formation in mouse embryos.
复制标题
engrailed-1 的反义靶向导致小鼠胚胎轴形成异常。
DOI：
10.1002/tera.1420510505
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
Augustine,KA
中科院分区：
文献类型：
--
作者：
Sadler,TW;Liu,ET;Augustine,KA
在早期体节小鼠胚胎中，针对enrailed-1（En-1）的反义寡核苷酸导致En蛋白水平降低，并导致大脑、面部和心脏异常以及胚胎轴缩短（尾部发育不全）。大脑和四肢的缺陷与其他研究者描述的无效突变小鼠中观察到的异常一致。面部和心脏的缺失可能与神经嵴细胞的改变有关。尾部发育不全表明En-1在轴形成中的作用，并且这一假设得到了原始条纹中存在En-1蛋白和mRNA的结果的支持。因此，除了参与大脑和肢体发育的信号传导途径外，En-1似乎在胚胎轴的形成中发挥作用。© 1995 Wiley利斯公司
Antisense oligonucleotide targeting ofengrailed‐1 (En‐1) in early somite mouse embryos resulted in reducedEnprotein levels and produced abnormalities of the brain, face, and heart and shortening of the embryonic axis (caudal dysgenesis). Defects of the brain and limbs were consistent with abnormalities observed in null mutant mice described by other investigators. Abnormalities of the face and heart may be related to alterations in neural crest cells. Caudal dysgenesis suggested a role forEn‐1in axis formation and this hypothesis was supported by results showing thatEn‐1 protein and mRNA are present in the primitive streak. Thus, in addition to participating in the signaling pathway for brain and limb development,En‐1 appears to play a role in patterning the embryonic axis. © 1995 Wiley‐Liss, Inc.