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SUMO 通路依赖性的细胞转录抑制因子在单纯疱疹病毒 1 基因组上的募集。

SUMO pathway dependent recruitment of cellular repressors to herpes simplex virus type 1 genomes.

机构信息

MRC-University of Glasgow Centre for Virus Research, Glasgow, Scotland, United Kingdom.

出版信息

PLoS Pathog. 2011 Jul;7(7):e1002123. doi: 10.1371/journal.ppat.1002123. Epub 2011 Jul 14.

DOI:10.1371/journal.ppat.1002123
PMID:21779164
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3136452/
Abstract

Components of promyelocytic leukaemia (PML) nuclear bodies (ND10) are recruited to sites associated with herpes simplex virus type 1 (HSV-1) genomes soon after they enter the nucleus. This cellular response is linked to intrinsic antiviral resistance and is counteracted by viral regulatory protein ICP0. We report that the SUMO interaction motifs of PML, Sp100 and hDaxx are required for recruitment of these repressive proteins to HSV-1 induced foci, which also contain SUMO conjugates and PIAS2β, a SUMO E3 ligase. SUMO modification of PML and elements of its tripartite motif (TRIM) are also required for recruitment in cells lacking endogenous PML. Mutants of PML isoform I and hDaxx that are not recruited to virus induced foci are unable to reproduce the repression of ICP0 null mutant HSV-1 infection mediated by their wild type counterparts. We conclude that recruitment of ND10 components to sites associated with HSV-1 genomes reflects a cellular defence against invading pathogen DNA that is regulated through the SUMO modification pathway.

摘要

早发性骨髓细胞性白血病（PML）核体（ND10）的组成部分在进入细胞核后不久就被招募到与单纯疱疹病毒 1 型（HSV-1）基因组相关的部位。这种细胞反应与内在的抗病毒抗性有关，并且受到病毒调节蛋白 ICP0 的拮抗。我们报告说，PML、Sp100 和 hDaxx 的 SUMO 相互作用基序是将这些抑制蛋白募集到 HSV-1 诱导焦点所必需的，这些焦点还包含 SUMO 缀合物和 PIAS2β，一种 SUMO E3 连接酶。PML 的 SUMO 修饰及其三联基序（TRIM）的元素对于在缺乏内源性 PML 的细胞中的募集也是必需的。不能募集到病毒诱导焦点的 PML 同种型 I 和 hDaxx 突变体不能复制其野生型对应物介导的 ICP0 缺失突变型 HSV-1 感染的抑制。我们得出结论，ND10 成分被招募到与 HSV-1 基因组相关的部位反映了一种针对入侵病原体 DNA 的细胞防御机制，该机制通过 SUMO 修饰途径进行调节。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/f6e162ca56bb/ppat.1002123.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/9f0d2642a09a/ppat.1002123.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/026301d58c71/ppat.1002123.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/0601c74a23ea/ppat.1002123.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/9ee3b608fc5f/ppat.1002123.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/6364689d00d3/ppat.1002123.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/842f2a621ab2/ppat.1002123.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/2580c5a74047/ppat.1002123.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/54dbda3476bf/ppat.1002123.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/598b678e1006/ppat.1002123.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/f6e162ca56bb/ppat.1002123.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/9f0d2642a09a/ppat.1002123.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/026301d58c71/ppat.1002123.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/0601c74a23ea/ppat.1002123.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/9ee3b608fc5f/ppat.1002123.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/6364689d00d3/ppat.1002123.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/842f2a621ab2/ppat.1002123.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/2580c5a74047/ppat.1002123.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/54dbda3476bf/ppat.1002123.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/598b678e1006/ppat.1002123.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5213/3136452/f6e162ca56bb/ppat.1002123.g010.jpg

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