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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Phage Φ29 Protein P56 Prevents Viral Dna Replication Impairment Caused By Uracil Excision Activity Of Uracil-dna Glycosylase
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Phage Φ29 Protein P56 Prevents Viral Dna Replication Impairment Caused By Uracil Excision Activity Of Uracil-dna Glycosylase

机译：噬菌体Φ29蛋白P56预防由于尿嘧啶-dna糖基化酶的尿嘧啶切除活性而引起的病毒dna复制障碍

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摘要

Protein p56 encoded by the Bacillus subtilis phage Φ29 inhibits host uracil-DNA glycosylase (UDG) activity. In previous studies, we suggested that this inhibition is likely a defense mechanism developed by phage Φ29 to prevent the action of UDG if uracilation occurs in DNA either from deamination of cytosine or the incorporation of dUMP during viral DNA replication. In this work, we analyzed the ability of Φ29 DNA polymerase to insert dUMP into DNA. Primer extension analysis showed that viral DNA polymerase incorporates dU opposite dA with a catalytic efficiency only 2-fold lower than that for dT. Using the Φ29 DNA amplification system, we found that Φ29 DNA polymerase is also able to carry out the extension of the dA:dUMP pair and replicate past uracil. Additionally, UDG and apurinic-apyrimidinic endonuclease treatment of viral DNA isolated from Φ29-infected cells revealed that uracil residues arise in Φ29 DNA during replication, probably as a result of misincorporation of dUMP by the Φ29 DNA polymerase. On the other hand, the action of UDG on uracil-containing Φ29 DNA impaired in vitro viral DNA replication, which was prevented by the presence of protein p56. Furthermore, transfection activity of uracil-containing Φ29 DNA was significantly higher in cells that constitutively synthesized p56 than in cells lacking this protein. Thus, our data support a model in which protein p56 ensures an efficient viral DNA replication, preventing the deleterious effect caused by UDG when it eliminates uracil residues present in the Φ29 genome.
机译：枯草芽孢杆菌噬菌体Φ29编码的蛋白p56抑制宿主尿嘧啶-DNA糖基化酶（UDG）的活性。在以前的研究中，我们认为这种抑制作用可能是噬菌体Φ29开发的一种防御机制，如果DNA中出现尿嘧啶脱氨作用或病毒DNA复制过程中dUMP的掺入，它可能阻止UDG的作用。在这项工作中，我们分析了Φ29DNA聚合酶将dUMP插入DNA的能力。引物延伸分析表明，病毒DNA聚合酶掺入了与dA相反的dU，其催化效率仅比dT低2倍。使用Φ29DNA扩增系统，我们发现Φ29DNA聚合酶也能够进行dA：dUMP对的延伸并复制通过尿嘧啶。此外，UDG和嘌呤-嘧啶二环内切酶对从Φ29感染细胞中分离的病毒DNA的处理显示，复制过程中Φ29DNA中出现尿嘧啶残基，这可能是由于Φ29DNA聚合酶误掺入dUMP所致。另一方面，UDG对含尿嘧啶的Φ29DNA的作用削弱了体外病毒DNA复制，这可以通过蛋白质p56的存在来阻止。此外，在组成性合成p56的细胞中，含尿嘧啶的Φ29DNA的转染活性明显高于缺乏该蛋白的细胞。因此，我们的数据支持了一个模型，其中蛋白质p56确保有效的病毒DNA复制，防止UD29消除Φ29基因组中存在的尿嘧啶残基而造成的有害作用。

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