Changes of the methylation pattern of the c-myc gene during in vitro aging of IMR90 human embryonic fibroblasts

Mutation Research/DNAging Pub Date : 1995-05-01 DOI:10.1016/0921-8734(95)90002-0

Jörn-Peter Halle , Claudia Schmidt , Gerold Adam

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引用次数: 14

Abstract

DNA modification by cytosine methylation has received considerable interest in the context of mammalian cell differentiation but is discussed controversially with respect to cellular aging. As the expression of c-myc affects strongly cellular aging and terminal differentiation, we have analysed the sequence-specific methylation pattern of the c-myc gene during proliferative aging in vitro of human embryonic fibroblasts. In this study, both, 5-methylcytidine sensitive restriction enzymes as well as genomic sequencing were used. The overall methylation pattern was found essentially stable during proliferative aging. However, specific hypermethylation of exon II during aging was observed. Futhermore, one specific cytidine located in the consensus sequence of the DNA binding factor PEBP2 was found completely methylated during most of the course of proliferative aging of the cells but became demethylated as the cells reached the end of their proliferative life span. Our results indicate the importance of establishing the sequence-specific changes of the methylation pattern of the genome during in vitro aging.

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IMR90人胚胎成纤维细胞体外衰老过程中c-myc基因甲基化模式的变化

在哺乳动物细胞分化的背景下，胞嘧啶甲基化引起的DNA修饰引起了相当大的兴趣，但在细胞衰老方面却存在争议。由于c-myc的表达强烈影响细胞衰老和终末分化，我们分析了体外人胚胎成纤维细胞增殖衰老过程中c-myc基因的序列特异性甲基化模式。在本研究中，使用了5-甲基胞苷敏感限制性内切酶和基因组测序。总体甲基化模式在增殖性衰老过程中基本稳定。然而，在衰老过程中观察到外显子II的特异性超甲基化。此外，发现位于DNA结合因子PEBP2共识序列中的一个特定胞苷在细胞增殖衰老的大部分过程中完全甲基化，但在细胞达到其增殖寿命结束时变为去甲基化。我们的结果表明，在体外衰老过程中建立基因组甲基化模式序列特异性变化的重要性。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Mutation Research/DNAging

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