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斑点和副斑点协调调节 HSV-1 基因转录。

Speckles and paraspeckles coordinate to regulate HSV-1 genes transcription.

机构信息

Department of Nuclear Medicine, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, 250014, China.

Biomedical Sciences College & Shandong Medicinal Biotechnology Centre, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, 250062, China.

出版信息

Commun Biol. 2021 Oct 21;4(1):1207. doi: 10.1038/s42003-021-02742-6.

DOI:10.1038/s42003-021-02742-6
PMID:34675360
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8531360/
Abstract

Numbers of nuclear speckles and paraspeckles components have been demonstrated to regulate herpes simplex virus 1 (HSV-1) replication. However, how HSV-1 infection affects the two nuclear bodies, and whether this influence facilitates the expression of viral genes, remains elusive. In the current study, we found that HSV-1 infection leads to a redistribution of speckles and paraspeckles components. Serine/arginine-rich splicing factor 2 (SRSF2), the core component of speckles, was associated with multiple paraspeckles components, including nuclear paraspeckles assembly transcript 1 (NEAT1), PSPC1, and P54nrb, in HSV-1 infected cells. This association coordinates the transcription of viral genes by binding to the promoters of these genes. By association with the enhancer of zeste homolog 2 (EZH2) and P300/CBP complex, NEAT1 and SRSF2 influenced the histone modifications located near viral genes. This study elucidates the interplay between speckles and paraspeckles following HSV-1 infection and provides insight into the mechanisms by which HSV-1 utilizes host cellular nuclear bodies to facilitate its life cycle.

摘要

核斑点和核旁斑点组件的数量已被证明可调节单纯疱疹病毒 1(HSV-1)的复制。然而,HSV-1 感染如何影响这两个核体,以及这种影响是否有助于病毒基因的表达,仍然难以捉摸。在本研究中,我们发现 HSV-1 感染导致斑点和核旁斑点组件重新分布。斑点的核心成分丝氨酸/精氨酸丰富剪接因子 2(SRSF2)与多个核旁斑点成分相关联,包括核旁斑点组装转录物 1(NEAT1)、PSPC1 和 P54nrb,在 HSV-1 感染的细胞中。这种关联通过与这些基因的启动子结合来协调病毒基因的转录。通过与增强子结合锌指蛋白 2(EZH2)和 P300/CBP 复合物的关联,NEAT1 和 SRSF2 影响位于病毒基因附近的组蛋白修饰。本研究阐明了 HSV-1 感染后斑点和核旁斑点之间的相互作用,并深入了解了 HSV-1 利用宿主细胞核体促进其生命周期的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c80b/8531360/55fc9d235f04/42003_2021_2742_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c80b/8531360/c03b3f45746f/42003_2021_2742_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c80b/8531360/e5c1d6d9c3c5/42003_2021_2742_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c80b/8531360/5dcbfd7a5128/42003_2021_2742_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c80b/8531360/0bc84ff15178/42003_2021_2742_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c80b/8531360/85cc9f34e570/42003_2021_2742_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c80b/8531360/55fc9d235f04/42003_2021_2742_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c80b/8531360/c03b3f45746f/42003_2021_2742_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c80b/8531360/e5c1d6d9c3c5/42003_2021_2742_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c80b/8531360/5dcbfd7a5128/42003_2021_2742_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c80b/8531360/0bc84ff15178/42003_2021_2742_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c80b/8531360/85cc9f34e570/42003_2021_2742_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c80b/8531360/55fc9d235f04/42003_2021_2742_Fig6_HTML.jpg

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