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感染蛙病毒3可使胞嘧啶而非腺嘌呤残基甲基化的DNA发生转录。

Infection with frog virus 3 allows transcription of DNA methylated at cytosine but not adenine residues.

作者信息

Thompson J P, Granoff A, Willis D B

出版信息

Virology. 1987 Sep;160(1):275-7. doi: 10.1016/0042-6822(87)90073-0.

Abstract

The genome of the iridovirus, frog virus 3, is highly methylated at cytosine residues by a virus-encoded DNA methyltransferase. We have shown previously that an FV3-induced trans-acting protein alters either host RNA polymerase II or methylated template to allow transcription from promoters inactivated by methylation. We now present evidence that the ability of FV3-infected cells to transcribe methylated DNA is specific for DNA methylated at cytosine residues. Eukaryotic promoters were inactivated by methylation of either adenine or cytosine residues, and tested for transcriptional activity. Only promoters inactivated by cytosine methylation were transcribed in FV3-infected cells. We also show that the dinucleotide sequence in which the methylcytosine is found appears to have no effect on the ability of FV3 to trans-activate the methylated promoters.

摘要

虹彩病毒蛙病毒3的基因组在胞嘧啶残基处被病毒编码的DNA甲基转移酶高度甲基化。我们之前已经表明,FV3诱导的反式作用蛋白会改变宿主RNA聚合酶II或甲基化模板,从而使甲基化失活的启动子能够进行转录。我们现在提供证据表明,FV3感染的细胞转录甲基化DNA的能力对胞嘧啶残基处甲基化的DNA具有特异性。通过腺嘌呤或胞嘧啶残基的甲基化使真核启动子失活,并测试其转录活性。只有被胞嘧啶甲基化失活的启动子在FV3感染的细胞中进行转录。我们还表明,发现甲基胞嘧啶的二核苷酸序列似乎对FV3反式激活甲基化启动子的能力没有影响。

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