<br>人赖氨酰-tRNA合成酶磷酸化促进HIV-1原病毒DNA转录,Nucleic Acids Research

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人赖氨酰-tRNA合成酶磷酸化促进HIV-1原病毒DNA转录
Nucleic Acids Research ( IF 16.6 ) Pub Date : 2023-11-07 , DOI: 10.1093/nar/gkad941
Yingke Tang _{1,

2,

3} , Ryan T Behrens ₄ , Corine St Gelais _{2,

3,

5} , Siqi Wu ₆ , Saravanan Vivekanandan ₇ , Ehud Razin ₈ , Pengfei Fang ₆ , Li Wu ₉ , Nathan Sherer ₄ , Karin Musier-Forsyth _{1,

2,

3}

Affiliation

Department of Chemistry and Biochemistry, Ohio State University, Columbus, OH, USA.
Center for Retrovirus Research, Ohio State University, Columbus, OH, USA.
Center for RNA Biology, Ohio State University, Columbus, OH, USA.
McArdle Laboratory for Cancer Research, Institute for Molecular Virology, & Carbone Cancer Center, University of Wisconsin, Madison, WI, USA.
Department of Veterinary Biosciences, Ohio State University, Columbus, OH, USA.
State Key Laboratory of Chemical Biology, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, China.
Cellular and Molecular Mechanisms of Inflammation Program, National University of Singapore and The Hebrew University of Jerusalem (NUS-HUJ), Singapore.
Department of Biochemistry and Molecular Biology, Institute for Medical Research Israel-Canada, The Hebrew University of Jerusalem, Israel.
Department of Microbiology and Immunology, Carver College of Medicine, University of Iowa, Iowa City, IA, USA.

此前研究表明，人赖氨酰-tRNA 合成酶 (LysRS) 从多氨酰基-tRNA 合成酶复合物 (MSC) 中的正常细胞质位置重新定位到 HIV-1 感染细胞的细胞核。核定位取决于 S207 磷酸化，但 pS207-LysRS 在 HIV-1 生命周期中的核功能尚不清楚。在这里，我们发现在 CRISPR/Cas9 生成的 S207A-LysRS 敲入细胞系中，HIV-1 复制严重减少； S207D-LysRS 挽救了这种效应。 LysRS 磷酸化上调 HIV-1 转录，直接转染 Ap4A 也是如此，Ap4A 是一种由 pS207-LysRS 合成的上游转录因子 2 (USF2) 激活剂。过度表达 MSC 衍生肽，已知可稳定 LysRS MSC 结合，从而抑制 HIV-1 复制。在表达肽的细胞中，HIV-1 前病毒 DNA 和其他 USF2 靶基因的转录减少。我们提出核 pS207-LysRS 生成 Ap4A，导致 HIV-1 转录激活。我们的结果表明核 LysRS 在促进 HIV-1 复制和抗病毒治疗的新途径方面具有新作用。

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更新日期：2023-11-07

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