Establishment of intestinal identity and epithelial-mesenchymal signaling by Cdx2.
Establishment of intestinal identity and epithelial-mesenchymal signaling by Cdx2.
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DOI：
10.1016/j.devcel.2009.02.010
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发表时间：
2009-04
影响因子：
11.8
通讯作者：
Kaestner, Klaus H.
中科院分区：
文献类型：
--
作者：
Gao, Nan;White, Peter;Kaestner, Klaus H.
我们证明，早期内胚层同源盒转录因子Cdx2的条件消融导致角化细胞取代后肠上皮，这是由前肠/食管分化程序的异位激活引起的戏剧性的细胞命运转换。当几个关键的前肠内胚层调控因子的表达向尾端转移时，这种前同质转化首先在胚胎早期cdx2缺陷肠道中表现明显。虽然肠道转录组受到严重影响，但cdx2缺陷仅短暂地修饰了选定的后端Hox基因，维持了主要的肠道Hox密码。此外，我们证明cdx2导向的肠细胞命运采用在正常上皮-间质相互作用的建立中起着重要作用，因为参与这一过程的多种信号通路受到严重影响。我们得出结论，Cdx2控制着肠道身份和发育的重要方面，并且这种功能在很大程度上独立于肠道Hox编码。
We demonstrate that conditional ablation of the homeobox transcription factor Cdx2 from early endoderm results in the replacement of the posterior intestinal epithelium with keratinocytes, a dramatic cell fate conversion caused by ectopic activation of the foregut/esophageal differentiation program. This anterior homeotic transformation is first evident in the early embryonic Cdx2-deficient gut as expression of several key foregut endoderm regulators was shifted caudally. While the intestinal transcriptome was severely affected, Cdx2-deficiency only transiently modified selected posterior Hox genes and the primary enteric Hox code was maintained. Further, we demonstrate that Cdx2-directed intestinal cell fate adoption plays an important role in the establishment of normal epithelial-mesenchymal interactions, as multiple signaling pathways involved in this process were severely affected. We conclude that Cdx2 controls important aspects of intestinal identity and development, and that this function is largely independent of the enteric Hox code.
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