Evolutionarily conserved requirement of Cdx for post-occipital tissue emergence
Evolutionarily conserved requirement of Cdx for post-occipital tissue emergence
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Cdx 对枕后组织出现的进化保守要求
DOI：
10.1242/dev.079848
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发表时间：
2012
期刊：
影响因子：
4.6
通讯作者：
J. Deschamps
中科院分区：
文献类型：
--
作者：
Carina van Rooijen;S. Simmini;M. Białecka;R. Neijts;C. van de Ven;F. Beck;J. Deschamps
小鼠Cdx基因参与轴向模式和部分Cdx突变体表现出后胚胎缺陷。我们发现，小鼠胚胎中，所有三个Cdx基因失活未能产生任何轴向组织以外的头和枕原基。在Cdx基因缺失的胚胎中，前轴组织被放置并形成良好的图案，并且3′ Hox基因最初在后脑中正常转录和表达。在没有Cdx的情况下，轴向伸长在后枕骨水平突然停止，因为后生长区失去了其祖细胞活性。外源性Fgf8挽救了Cdx突变体的后截短，并且Cdx无效胚胎的缺陷谱与后Fgfr 1信号丢失所导致的缺陷谱相匹配。我们的数据认为，Cdx的主要功能，在执行躯干出现以外的Cdx独立的头枕区，并为下游的Fgfr 1信号在此功能的作用。Cdx的要求后头部部分的轴是祖先，因为它发生在节肢动物以及。
Mouse Cdx genes are involved in axial patterning and partial Cdx mutants exhibit posterior embryonic defects. We found that mouse embryos in which all three Cdx genes are inactivated fail to generate any axial tissue beyond the cephalic and occipital primordia. Anterior axial tissues are laid down and well patterned in Cdx null embryos, and a 3′ Hox gene is initially transcribed and expressed in the hindbrain normally. Axial elongation stops abruptly at the post-occipital level in the absence of Cdx, as the posterior growth zone loses its progenitor activity. Exogenous Fgf8 rescues the posterior truncation of Cdx mutants, and the spectrum of defects of Cdx null embryos matches that resulting from loss of posterior Fgfr1 signaling. Our data argue for a main function of Cdx in enforcing trunk emergence beyond the Cdx-independent cephalo-occipital region, and for a downstream role of Fgfr1 signaling in this function. Cdx requirement for the post-head section of the axis is ancestral as it takes place in arthropods as well.