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首页> 外文期刊>Molecular and Cellular Biology >Induction of alpha-fetoprotein synthesis in differentiating F9 teratocarcinoma cells is accompanied by a genome-wide loss of DNA methylation.
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Induction of alpha-fetoprotein synthesis in differentiating F9 teratocarcinoma cells is accompanied by a genome-wide loss of DNA methylation.

机译：在分化的F9畸胎瘤细胞中诱导甲胎蛋白的合成伴随着全基因组DNA甲基化的丧失。

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F9 teratocarcinoma cells can be grown as monolayers or aggregates, and upon treatment with retinoic acid they will differentiate into parietal or visceral endoderm, respectively. Visceral endoderm specifically synthesizes alpha-fetoprotein and albumin mRNAs, which are not found in parietal endoderm. In contrast, both endoderms produce enhanced levels of the major histocompatibility antigen (H2) mRNA compared with F9 cells. F9 cells contain highly methylated DNA as judged by restriction enzyme digestion. However, upon differentiation into visceral endoderm, there is a genome-wide loss of methylation in induced, silent, and constitutively expressed genes. Experiments in which methylation loss is induced via the methyltransferase inhibitor 5-azacytidine result in no induction of alpha-fetoprotein mRNA and no morphological differentiation, suggesting that methylation loss alone is not sufficient to induce the visceral endoderm phenotype. Likewise, 5-azacytidine treatment of differentiated cells does not result in enhanced expression of alpha-fetoprotein mRNA. However, the patterns of loss of DNA methylation at all sites examined after differentiation or 5-azacytidine treatment were remarkably similar, suggesting that the two occur by a similar mechanism, the inhibition of DNA methyltransferase activity. These results argue that the specificity for methylation loss at a given site is an inherent property of aggregated F9 cell chromatin. This system provides a model for studying a tissue-specific change in DNA methylation upon differentiation.
机译：F9畸胎瘤细胞可以单层或聚集体形式生长，并且在使用视黄酸处理后，它们将分别分化为顶内膜或内脏内胚层。内脏内胚层特异性合成顶叶内胚层中未发现的甲胎蛋白和白蛋白mRNA。相比之下，与F9细胞相比，两种内胚层均产生增强的主要组织相容性抗原（H2）mRNA。通过限制性酶消化判断，F9细胞含有高度甲基化的DNA。但是，在分化成内脏内胚层后，在诱导，沉默和组成性表达的基因中全基因组范围内的甲基化损失。通过甲基转移酶抑制剂5-氮杂胞苷诱导甲基化损失的实验未诱导甲胎蛋白的表达，也没有形态学上的分化，提示仅甲基化损失不足以诱导内脏内胚层表型。同样，对分化细胞进行5-氮杂胞苷处理不会导致甲胎蛋白mRNA的表达增强。然而，在分化或5-氮杂胞苷处理后检查的所有位点，DNA甲基化损失的模式非常相似，表明这两者是通过相似的机制发生的，即抑制DNA甲基转移酶活性。这些结果表明，给定位点甲基化损失的特异性是聚集的F9细胞染色质的固有特性。该系统提供了用于研究分化后DNA甲基化的组织特异性变化的模型。

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