Effect of HDAC9-induced deacetylation of glycolysis-related GAPDH lysine 219 on rotavirus replication in rotavirus-infected Caco-2 cells.

IF 1.9 4区医学 Q3 GENETICS & HEREDITY

Virus Genes Pub Date : 2024-12-01 Epub Date: 2024-09-20 DOI:10.1007/s11262-024-02104-4

Lijun Song, Peicheng Zhong, Runyu Yu, Yue Yuan, Yujing Zhou, Yupei Qian, Siyan Yang, Haosen Yi, Zhiyan Yang, Wenchang Zhao

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引用次数: 0

Abstract

Post-translational modifications (PTMs), as epigenetic modifications, are significant in the interaction between virus and its host. However, it is unclear whether rotavirus (RV) causes changes in both the host cell epigenetic protein modification and the regulatory mechanism of viral replication. Here, we analyzed the proteome of Caco-2 cells to determine if acetylation modification occurred within the cells after RV infection. We found that glyceraldehyde-3-phosphate dehydrogenase (GAPDH), a protein involved in glycolysis, was deacetylated at lysine 219 via histone deacetylase 9 (HDAC9) in 50 h after the RV infection. Remarkably, the deacetylation of GAPDH promoted RV replication. Finally, we found that glycolysis was alterable in Caco-2 cells by RV or the deacetylation of GAPDH lysine 219, using the Seahorse XF Glycolysis Stress Test. In conclusion, our results demonstrate for the first time that RV infection promoted deacetylation of GAPDH at lysine 219 in order to increase its own viral replication in Caco-2 cells.

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HDAC9 诱导的糖酵解相关 GAPDH 赖氨酸 219 去乙酰化对轮状病毒感染的 Caco-2 细胞中轮状病毒复制的影响。

翻译后修饰（PTM）作为表观遗传修饰，在病毒与其宿主的相互作用中具有重要意义。然而，目前还不清楚轮状病毒（RV）是否会导致宿主细胞表观遗传蛋白质修饰和病毒复制调控机制发生变化。在此，我们分析了 Caco-2 细胞的蛋白质组，以确定 RV 感染后细胞内是否发生了乙酰化修饰。我们发现，参与糖酵解的甘油醛-3-磷酸脱氢酶（GAPDH）在感染 RV 50 小时后通过组蛋白去乙酰化酶 9（HDAC9）在赖氨酸 219 处发生了去乙酰化。值得注意的是，GAPDH的去乙酰化促进了RV的复制。最后，我们利用海马 XF 糖酵解压力测试（Seahorse XF Glycolysis Stress Test）发现，RV 或 GAPDH 赖氨酸 219 的去乙酰化可改变 Caco-2 细胞中的糖酵解。总之，我们的研究结果首次证明了 RV 感染会促进 GAPDH 在赖氨酸 219 处的去乙酰化，从而增加其自身病毒在 Caco-2 细胞中的复制。

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

Virus Genes 医学-病毒学

CiteScore

3.30

自引率

0.00%

发文量

审稿时长

3 months

期刊介绍： Viruses are convenient models for the elucidation of life processes. The study of viruses is again on the cutting edge of biological sciences: systems biology, genomics, proteomics, metagenomics, using the newest most powerful tools. Huge amounts of new details on virus interactions with the cell, other pathogens and the hosts – animal (including human), insect, fungal, plant, bacterial, and archaeal - and their role in infection and disease are forthcoming in perplexing details requiring analysis and comments. Virus Genes is dedicated to the publication of studies on the structure and function of viruses and their genes, the molecular and systems interactions with the host and all applications derived thereof, providing a forum for the analysis of data and discussion of its implications, and the development of new hypotheses.