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人 TAT 特异性因子 1 结合 HIV-1 基因组,并选择性地转运 HIV-1 RNA。

Human Tat-specific factor 1 binds the HIV-1 genome and selectively transports HIV-1 RNAs.

机构信息

Biochemistry and Molecular Biology Program, University of Rochester Medical Center, Rochester, NY, 14627, USA.

Department of Biology, High Point University, High Point, NC, 27268, USA.

出版信息

Mol Biol Rep. 2020 Mar;47(3):1759-1772. doi: 10.1007/s11033-020-05267-z. Epub 2020 Feb 3.

Abstract

Human immunodeficiency virus type 1 (HIV-1) propagation requires many human cofactors. Multiple groups have demonstrated that Tat-specific factor 1 (Tat-SF1) is an HIV-1 dependency factor. Depletion of this protein lowers HIV-1 infectivity, however, it does not affect the overall levels of viral RNA. Rather, Tat-SF1 regulates the relative levels of each RNA size class. This would be consistent with roles in splicing, transport, and/or stability of viral RNAs. We hypothesized that if Tat-SF1 plays any of these roles, then we should detect binding of the protein to the RNA genome. Furthermore, knocking down Tat-SF1 should result in altered RNA stability and/or localization in human cells. Fragments of the HIV-1 genome were used as RNA probes in electrophoretic mobility shift assays and fluorescence correlation spectroscopy experiments. Our results show that Tat-SF1 can form a complex with TAR RNA in vitro, independent of Tat. This factor interacts with at least one additional location in the 5' end of the HIV-1 genome. Tat seems to enhance the formation of this complex. To analyze HIV-1 RNA localization, HeLa cells with Tat-SF1 knocked down were also transfected with a proviral clone. RNA from nuclear and cytoplasmic fractions was purified, followed by RT-qPCR analysis. Tat-SF1 likely binds the HIV-1 RNA genome at TAR and potentially other locations and selectively transports HIV-1 RNAs, facilitating the unspliced RNA's nuclear export while retaining singly spliced RNAs in the nucleus. This is a novel role for this HIV-1 dependency factor.

摘要

人类免疫缺陷病毒 1 型(HIV-1)的传播需要多种人类辅助因子。多个研究小组已经证明,Tat 特异性因子 1(Tat-SF1)是 HIV-1 的依赖因子。该蛋白的耗竭降低了 HIV-1 的感染性,但不会影响病毒 RNA 的总水平。相反,Tat-SF1 调节每个 RNA 大小类别的相对水平。这与 RNA 的剪接、运输和/或稳定性有关。我们假设,如果 Tat-SF1 发挥这些作用中的任何一种作用,那么我们应该检测到该蛋白与 RNA 基因组的结合。此外,敲低 Tat-SF1 应该导致 RNA 稳定性和/或在人类细胞中的定位改变。使用 HIV-1 基因组的片段作为 RNA 探针进行电泳迁移率变动分析和荧光相关光谱实验。我们的结果表明,Tat-SF1 可以在体外与 TAR RNA 形成复合物,而无需 Tat。该因子与 HIV-1 基因组 5' 端的至少另一个位置相互作用。 Tat 似乎增强了该复合物的形成。为了分析 HIV-1 RNA 的定位,用 Tat-SF1 敲低的 HeLa 细胞也转染了前病毒克隆。纯化核和细胞质部分的 RNA,然后进行 RT-qPCR 分析。Tat-SF1 可能在 TAR 及其他潜在位置结合 HIV-1 RNA 基因组,并选择性地转运 HIV-1 RNA,促进未剪接 RNA 的核输出,同时将单剪接 RNA 保留在核内。这是这种 HIV-1 依赖性因子的新作用。

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