SAP30 deacetylates the Tas protein to inhibit PFV replication.

IF 6.1 2区生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Cell and Bioscience Pub Date : 2025-04-24 DOI:10.1186/s13578-025-01400-2

Chenchen Wang, Junshi Zhang, Yali Xu, Jiawei Zhao, Manman Qiu, Xingli Zhao, Guoqiang Li, Wentao Qiao, Juan Tan

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引用次数: 0

Abstract

Background: Foamy viruses (FVs), a unique class of retroviruses, establish lifelong latent infections in the host without causing symptoms, contributing to the relatively slow progress in FV research. However, key mutations in FVs can result in severe consequences due to their broad cellular tropism, underscoring the importance of studying latent FV infections.

Results: To identify new host proteins involved in the replication of prototype foamy virus (PFV), we previously infected the human fibrosarcoma cell line HT1080 with PFV and performed transcriptomic sequencing. The analysis revealed a significant upregulation of SAP30 mRNA levels following PFV infection. Further experiments demonstrated that PFV infection enhances SAP30 promoter activity via the Tas protein, leading to increased SAP30 mRNA and protein expression. Overexpression of SAP30 inhibited PFV replication, whereas knockdown of endogenous SAP30 enhanced PFV replication. Furthermore, SAP30 interacted with the Tas protein to induce its deacetylation, thereby suppressing Tas-mediated transactivation of the PFV LTR and IP promoters. The Sin3 interaction domain at the C-terminus of SAP30 was identified as the critical domain for inhibiting PFV transcription.

Conclusions: Our findings suggest that SAP30 inhibits PFV replication by deacetylating the Tas protein, thereby disrupting its transcriptional activation function.

Key words: prototype foamy virus; SAP30; Tas; transcription; deacetylation.

查看原文本刊更多论文

SAP30使Tas蛋白去乙酰化以抑制PFV复制。

背景：泡沫病毒（virus, FVs）是一类独特的逆转录病毒，在宿主体内建立终身潜伏感染而不引起症状，导致FV研究进展相对缓慢。然而，由于其广泛的细胞趋向性，FV的关键突变可能导致严重的后果，这强调了研究潜伏性FV感染的重要性。结果：为了鉴定参与原型泡沫病毒（PFV）复制的新宿主蛋白，我们先前用PFV感染了人纤维肉瘤细胞系HT1080，并进行了转录组测序。分析显示，PFV感染后SAP30 mRNA水平显著上调。进一步的实验表明，PFV感染通过Tas蛋白增强SAP30启动子活性，导致SAP30 mRNA和蛋白表达增加。SAP30的过表达抑制了PFV的复制，而内源性SAP30的敲低则增强了PFV的复制。此外，SAP30与Tas蛋白相互作用诱导其去乙酰化，从而抑制Tas介导的PFV LTR和IP启动子的转激活。SAP30 c端Sin3相互作用结构域是抑制PFV转录的关键结构域。结论：我们的研究结果表明，SAP30通过使Tas蛋白去乙酰化来抑制PFV复制，从而破坏其转录激活功能。关键词：原型泡沫病毒；SAP30;助教;转录;脱乙酰作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cell and Bioscience BIOCHEMISTRY & MOLECULAR BIOLOGY-

CiteScore

10.70

自引率

0.00%

发文量

187

审稿时长

>12 weeks

期刊介绍： Cell and Bioscience, the official journal of the Society of Chinese Bioscientists in America, is an open access, peer-reviewed journal that encompasses all areas of life science research.