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PRMT1调节可变剪接以增强HPV18 mRNA稳定性并促进感染的建立。

PRMT1 Modulates Alternative Splicing to Enhance HPV18 mRNA Stability and Promote the Establishment of Infection.

作者信息

Williams David E J, King Kelly, Jackson Robert, Kuehner Franziska, Arnoldy Christina, Marroquin Jaclyn N, Tobey Isabelle, Banka Amy, Ragonese Sofia, Van Doorslaer Koenraad

机构信息

Cancer Biology Graduate Interdisciplinary Program, University of Arizona, Tucson, Arizona, USA.

Medical Scientist Training M.D.-Ph.D. Program, University of Arizona, Tucson, AZ, USA.

出版信息

bioRxiv. 2024 Sep 26:2024.09.26.614592. doi: 10.1101/2024.09.26.614592.

Abstract

Only persistent HPV infections lead to the development of cancer. Thus, understanding the virus-host interplay that influences the establishment of viral infection has important implications for HPV biology and human cancers. The ability of papillomaviruses to establish in cells requires the strict temporal regulation of viral gene expression in sync with cellular differentiation. This control primarily happens at the level of RNA splicing and polyadenylation. However, the details of how this spatio-temporal regulation is achieved still need to be fully understood. Until recently, it has been challenging to study the early events of the HPV lifecycle following infection. We used a single-cell genomics approach to identify cellular factors involved in viral infection and establishment. We identify protein arginine N-methyltransferase 1 (PRMT1) as an important factor in viral infection of primary human cervical cells. PRMT1 is the main cellular enzyme responsible for asymmetric dimethylation of cellular proteins. PRMT1 is an enzyme responsible for catalyzing the methylation of arginine residues on various proteins, which influences processes such as RNA processing, transcriptional regulation, and signal transduction. In this study, we show that HPV18 infection leads to increased PRMT1 levels across the viral lifecycle. PRMT1 is critical for the establishment of a persistent infection in primary cells. Mechanistically, PRMT1 inhibition leads to a highly dysregulated viral splicing pattern. Specifically, reduced PRMT1 activity leads to intron retention and a change in the E6 and E7 expression ratio. In the absence of PRMT1, viral transcripts are destabilized and subject to degradation via the nonsense-mediated decay (NMD) pathway. These findings highlight PRMT1 as a critical regulator of the HPV18 lifecycle, particularly in RNA processing, and position it as a potential therapeutic target for persistent HPV18 infections.

摘要

只有持续性人乳头瘤病毒(HPV)感染才会导致癌症的发生。因此,了解影响病毒感染建立的病毒与宿主之间的相互作用,对HPV生物学和人类癌症具有重要意义。乳头瘤病毒在细胞中建立感染的能力需要病毒基因表达与细胞分化严格同步的时间调控。这种调控主要发生在RNA剪接和多聚腺苷酸化水平。然而,这种时空调控是如何实现的细节仍有待充分了解。直到最近,研究HPV感染后生命周期的早期事件一直具有挑战性。我们使用单细胞基因组学方法来确定参与病毒感染和建立的细胞因子。我们确定蛋白质精氨酸N-甲基转移酶1(PRMT1)是原代人宫颈细胞病毒感染中的一个重要因子。PRMT1是负责细胞蛋白不对称二甲基化的主要细胞酶。PRMT1是一种负责催化各种蛋白质上精氨酸残基甲基化的酶,它影响RNA加工、转录调控和信号转导等过程。在本研究中,我们表明HPV18感染在整个病毒生命周期中导致PRMT1水平升高。PRMT1对原代细胞中持续性感染的建立至关重要。从机制上讲,PRMT1抑制导致病毒剪接模式高度失调。具体而言,PRMT1活性降低导致内含子保留以及E6和E7表达比例的变化。在没有PRMT1的情况下,病毒转录本不稳定,并通过无义介导的衰变(NMD)途径被降解。这些发现突出了PRMT1作为HPV18生命周期的关键调节因子,特别是在RNA加工方面,并将其定位为持续性HPV18感染的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4af/11463397/5f326ec62e11/nihpp-2024.09.26.614592v1-f0001.jpg

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