Comparative study of Msx-1 expression in early normal and vitamin A-deficient avian embryos.

Comparative study of Msx-1 expression in early normal and vitamin A-deficient avian embryos.
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早期正常和维生素 A 缺乏的禽胚胎中 Msx-1 表达的比较研究。

DOI:
10.1002/jez.1402720408
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发表时间:
1995
期刊:
The Journal of experimental zoology.
影响因子:
--
通讯作者:
Solursh,M
Solursh,M
中科院分区:
--
文献类型:
--
作者:
Chen,Y;Kostetskii,I;Zile,MH;Solursh,M

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含有同源框的基因可能在脊椎动物发育过程中建立胚胎模式中发挥重要作用。视黄酸能够诱导培养细胞中Hox基因的表达,并改变发育中脊椎动物胚胎的表达模式。利用全胚胎原位杂交技术,我们检测并比较了含同源盒基因Msx-1在早期正常和维生素A缺乏鹌鹑胚胎中的表达模式。在原肠胚形成阶段,Msx-1主要在正常和维生素A缺乏胚胎的后半部分表达。然而,该基因在缺乏维生素A的胚胎中表达更广泛和更强。在神经形成阶段,Msx-1在正常和维生素A缺乏的胚胎中,在后部区域直到亨森结和神经褶皱的边缘持续表达。值得注意的是,在维生素A缺乏的胚胎中,Msx-1表达更强,并且在前部和心前区异位表达。这些结果提供了证据,表明内源性类维生素A参与了Msx-1在鸟类胚胎中的正常表达,并且在早期鸟类胚胎发生过程中,Msx-1的表达在体内被内源性和生理性类维生素A下调。© 1995 Wiley利斯公司
Homeobox‐containing genes may play an important role in establishing embryonic patterns during development of vertebrates. Retinoic acid is able to induce expression of Hox genes in cells in culture and to alter expression patterns in the developing vertebrate embryos. Using wholemount in situ hybridization, we have examined and compared the expression patterns of a homeobox‐containing gene, Msx‐1, in early normal and vitamin A‐deficient quail embryos. At gastrulation stage, Msx‐1 is primarily expressed in the posterior half of both normal and vitamin A‐deficient embryos. However, the gene is expressed wider and stronger in the vitamin A‐deficient embryos. At neurulation stages, Msx‐1 is continuously expressed in the posterior region up to Hensen's node and in the edge of the neural fold in both normal and vitamin A‐deficient embryos. Notably, in the vitamin A‐deficient embryos, Msx‐1 is expressed more strongly and is also expressed ectopically in the anterior and precardiac regions. These results provide evidence that endogenous retinoids are involved in the normal expression of Msx‐1 in avian embryo and that the expression of Msx‐1 is downregulated by endogenous and physiological retinoids in vivo during early avian embryogenesis. © 1995 Wiley‐Liss, Inc.
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