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首页> 外文期刊>Genomics >Striking differences between the mouse and the human alpha-fetoprotein enhancers.
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Striking differences between the mouse and the human alpha-fetoprotein enhancers.

机译：小鼠和人类甲胎蛋白增强子之间的惊人差异。

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摘要

The alpha-fetoprotein (AFP) gene is expressed abundantly in the fetal liver and transcriptionally repressed in the adult liver, but can be reactivated during liver regeneration and in liver tumors. Previous studies identified three enhancers, E1, E2, and E3, upstream of the mouse and rat Afp genes and a single enhancer upstream of the human gene. We have compared the sequences upstream of the rodent and primate AFP genes. Our analysis demonstrates that the previously identified human enhancer is the counterpart to mouse E2. This comparison also reveals that a functional primate counterpart to the rodent E1 is absent due to a deletion that removes the core region of this enhancer. Furthermore, our studies identify a novel human enhancer corresponding to rodent E3. Despite the overall similarity of E3 between human and mouse, we found differences in transcription factor binding sites between these species. A C/EBP binding site is conserved but two other motifs in rodent E3, one that binds orphan nuclear receptors and a second that binds FoxA proteins, are not conserved in humans. The human counterpart to the rodent FoxA site can bind COUP-TF factors. Despite the overall sequence similarity in E3 between mice and humans, the difference in factor binding sites in E3, as well as the absence of E1 in primates, indicates that different mechanisms regulate AFP transcription in these different species.
机译：甲胎蛋白（AFP）基因在胎儿肝脏中大量表达，在成年肝脏中转录抑制，但可以在肝再生和肝肿瘤中重新激活。先前的研究在小鼠和大鼠Afp基因的上游鉴定了三个增强子E1，E2和E3，在人类基因的上游鉴定了单个增强子。我们已经比较了啮齿动物和灵长类动物AFP基因上游的序列。我们的分析表明，先前鉴定的人类增强子与小鼠E2相对。该比较还表明，由于缺失去除了该增强子的核心区域，因此缺少与啮齿动物E1对应的功能灵长类。此外，我们的研究确定了一种新型的人类增强剂，与啮齿动物E3相对应。尽管E3在人类和小鼠之间总体相似，但我们发现这些物种之间在转录因子结合位点方面存在差异。 C / EBP结合位点是保守的，但啮齿动物E3中的两个其他基序在人类中却不保守，一个结合孤儿核受体，另一个结合FoxA蛋白。啮齿动物FoxA位点的人类对应物可以结合COUP-TF因子。尽管小鼠和人之间E3在序列上总体相似，但E3中因子结合位点的差异以及灵长类动物中E1的缺失表明，不同的机制调节了这些不同物种中的AFP转录。

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