持续性人博尔纳病病毒感染使人类少突胶质细胞的乙酰化蛋白质组向更高的能量和转运体水平转变。
Persistent human Borna disease virus infection modifies the acetylome of human oligodendroglia cells towards higher energy and transporter levels.
作者信息
Liu Xia, Liu Siwen, Bode Liv, Liu Chengyu, Zhang Liang, Wang Xiao, Li Dan, Lei Yang, Peng Xiaojun, Cheng Zhongyi, Xie Peng
机构信息
Shanghai Key Laboratory of Forensic Medicine, Institute of Forensic Science, Ministry of Justice, Shanghai 200063, China.
Institute of Neuroscience and the Collaborative Innovation Center for Brain Science, Chongqing Medical University, Chongqing 400016, China; Chongqing Key Laboratory of Neurobiology, Chongqing Medical University, Chongqing 400016, China.
出版信息
Virology. 2015 Nov;485:58-78. doi: 10.1016/j.virol.2015.06.024. Epub 2015 Jul 23.
BACKGROUND
Borna disease virus (BDV) is a neurotropic RNA virus persistently infecting mammalian hosts including humans. Lysine acetylation (Kac) is a key protein post-translational modification (PTM). The unexpectedly broad regulatory scope of Kac let us to profile the entire acetylome upon BDV infection.
METHODS
The acetylome was profiled through stable isotope labeling for cell culture (SILAC)-based quantitative proteomics. The quantifiable proteome was annotated using bioinformatics.
RESULTS
We identified and quantified 791 Kac sites in 473 Kac proteins in human BDV Hu-H1-infected and non-infected oligodendroglial (OL) cells. Bioinformatic analysis revealed that BDV infection alters the acetylation of metabolic proteins, membrane-associated proteins and transmembrane transporter activity, and affects the acetylation of several lysine acetyltransferases (KAT).
CONCLUSIONS
Upon BDV persistence the OL acetylome is manipulated towards higher energy and transporter levels necessary for shuttling BDV proteins to and from nuclear replication sites.
背景
博尔纳病病毒（BDV）是一种嗜神经RNA病毒，可持续感染包括人类在内的哺乳动物宿主。赖氨酸乙酰化（Kac）是一种关键的蛋白质翻译后修饰（PTM）。Kac出人意料的广泛调控范围促使我们对BDV感染后的整个乙酰化蛋白质组进行分析。
方法
通过基于细胞培养的稳定同位素标记（SILAC）定量蛋白质组学对乙酰化蛋白质组进行分析。使用生物信息学对可定量的蛋白质组进行注释。
结果
我们在人BDV Hu-H1感染和未感染的少突胶质细胞（OL）中鉴定并定量了473个Kac蛋白中的791个Kac位点。生物信息学分析表明，BDV感染会改变代谢蛋白、膜相关蛋白的乙酰化以及跨膜转运蛋白活性，并影响几种赖氨酸乙酰转移酶（KAT）的乙酰化。
结论
在BDV持续感染时，OL乙酰化蛋白质组会朝着将BDV蛋白往返于核复制位点所需的更高能量和转运水平进行调控。
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