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首页> 外文期刊>Molecular and Cellular Biology >Intestinal Master Transcription Factor CDX2 Controls Chromatin Access for Partner Transcription Factor Binding
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Intestinal Master Transcription Factor CDX2 Controls Chromatin Access for Partner Transcription Factor Binding

机译：肠道主要转录因子CDX2控制染色质对伴侣转录因子结合的访问。

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Tissue-specific gene expression requires modulation of nucleosomes, allowing transcription factors to occupy cis elements that are accessible only in selected tissues. Master transcription factors control cell-specific genes and define cellular identities, but it is unclear if they possess special abilities to regulate cell-specific chromatin and if such abilities might underlie lineage determination and maintenance. One prevailing view is that several transcription factors enable chromatin access in combination. The homeodomain protein CDX2 specifies the embryonic intestinal epithelium, through unknown mechanisms, and partners with transcription factors such as HNF4A in the adult intestine. We examined enhancer chromatin and gene expression following Cdx2 or Hnf4a excision in mouse intestines. HNF4A loss did not affect CDX2 binding or chromatin, whereas CDX2 depletion modified chromatin significantly at CDX2-bound enhancers, disrupted HNF4A occupancy, and abrogated expression of neighboring genes. Thus, CDX2 maintains transcription-permissive chromatin, illustrating a powerful and dominant effect on enhancer configuration in an adult tissue. Similar, hierarchical control of cell-specific chromatin states is probably a general property of master transcription factors.
机译：组织特异性基因表达需要调节核小体，使转录因子占据仅在选定组织中可访问的 cis 元件。主转录因子控制细胞特异性基因并定义细胞身份，但尚不清楚它们是否具有调节细胞特异性染色质的特殊能力，以及这些能力是否可能作为谱系确定和维持的基础。一种流行的观点是，几种转录因子可以联合使用染色质。同源结构域蛋白CDX2通过未知机制指定了胚胎肠道上皮，并与成年肠道中的转录因子（例如HNF4A）结合。我们检查了小鼠肠中 Cdx2 或 Hnf4a 切除后的染色质增强子和基因表达。 HNF4A丢失不会影响CDX2结合或染色质，而CDX2耗竭会显着修饰CDX2结合的增强子上的染色质，破坏HNF4A的占有，并废除邻近基因的表达。因此，CDX2维持转录允许的染色质，说明在成人组织中对增强子构型的强大和显性作用。类似地，细胞特异性染色质状态的分级控制可能是主转录因子的一般属性。

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