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EHMT1N 的细胞质形式甲基化病毒蛋白，以促进包含体成熟和有效的病毒复制。

A cytoplasmic form of EHMT1N methylates viral proteins to enable inclusion body maturation and efficient viral replication.

机构信息

Council of Scientific and Industrial Research (CSIR)-Institute of Genomics and Integrative Biology (IGIB), New Delhi, India.

Academy of Scientific and Innovative Research (AcSIR), Ghaziabad; India.

出版信息

PLoS Biol. 2024 Nov 7;22(11):e3002871. doi: 10.1371/journal.pbio.3002871. eCollection 2024 Nov.

DOI:10.1371/journal.pbio.3002871
PMID:39509467
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11575796/
Abstract

Protein lysine methyltransferases (PKMTs) methylate histone and non-histone proteins to regulate biological outcomes such as development and disease including viral infection. While PKMTs have been extensively studied for modulating the antiviral responses via host gene regulation, their role in methylation of proteins encoded by viruses and its impact on host-pathogen interactions remain poorly understood. In this study, we discovered distinct nucleo-cytoplasmic form of euchromatic histone methyltransferase 1 (EHMT1N/C), a PKMT, that phase separates into viral inclusion bodies (IBs) upon cytoplasmic RNA-virus infection (Sendai Virus). EHMT1N/C interacts with cytoplasmic EHMT2 and methylates SeV-Nucleoprotein upon infection. Elevated nucleoprotein methylation during infection correlated with coalescence of small IBs into large mature platforms for efficient replication. Inhibition of EHMT activity by pharmacological inhibitors or genetic depletion of EHMT1N/C reduced the size of IBs with a concomitant reduction in replication. Additionally, we also found that EHMT1 condensation is not restricted to SeV alone but was also seen upon pathogenic RNA viral infections caused by Chandipura and Dengue virus. Collectively, our work elucidates a new mechanism by which cytoplasmic EHMT1 acts as proviral host factor to regulate host-pathogen interaction.

摘要

蛋白赖氨酸甲基转移酶（PKMTs）可使组蛋白和非组蛋白发生甲基化，从而调节生物过程，如发育和疾病（包括病毒感染）。尽管 PKMTs 已被广泛研究用于通过宿主基因调控来调节抗病毒反应，但它们在病毒编码蛋白的甲基化及其对宿主-病原体相互作用的影响方面的作用仍知之甚少。在这项研究中，我们发现了一种独特的核质形式的常染色质组蛋白甲基转移酶 1（EHMT1N/C），它是一种 PKMT，在细胞质 RNA 病毒感染（仙台病毒）时会相分离到病毒包含体（IB）中。EHMT1N/C 与细胞质中的 EHMT2 相互作用，并在感染时甲基化 SeV-N 蛋白。感染过程中核蛋白甲基化水平升高与小 IB 融合成大成熟平台以进行有效复制有关。EHMT 活性的药理学抑制剂抑制或 EHMT1N/C 的基因耗竭均可减小 IB 的大小，同时降低复制效率。此外，我们还发现，EHMT1 的浓缩不仅局限于 SeV，还发生在 Chandipura 和登革热等致病性 RNA 病毒感染中。总之，我们的工作阐明了细胞质 EHMT1 作为辅助病毒宿主因子调节宿主-病原体相互作用的新机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/566ef0fde86d/pbio.3002871.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/b5e2e5d02b30/pbio.3002871.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/fadbe7ef1fc2/pbio.3002871.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/d5743c28eaf3/pbio.3002871.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/d5f32f357114/pbio.3002871.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/15bf66264239/pbio.3002871.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/353e3ec6234d/pbio.3002871.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/71f2ae796a44/pbio.3002871.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/0cf3ab458f05/pbio.3002871.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/8a5dd848a21f/pbio.3002871.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/566ef0fde86d/pbio.3002871.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/b5e2e5d02b30/pbio.3002871.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/fadbe7ef1fc2/pbio.3002871.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/d5743c28eaf3/pbio.3002871.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/d5f32f357114/pbio.3002871.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/15bf66264239/pbio.3002871.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/353e3ec6234d/pbio.3002871.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/71f2ae796a44/pbio.3002871.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/0cf3ab458f05/pbio.3002871.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/8a5dd848a21f/pbio.3002871.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5ee8/11575796/566ef0fde86d/pbio.3002871.g010.jpg

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