Ph.D. Program in Humanics, School of Integrative and Global Majors, University of Tsukuba, Japan.
Faculty of Medicine, University of Tsukuba, Japan.
FEBS J. 2020 Jan;287(1):205-217. doi: 10.1111/febs.15027. Epub 2019 Aug 9.
The adenovirus (Ad) genome is believed to be packaged into the virion by forming a chromatin-like structure. The replicated viral genome is likely to be condensed through binding with viral core proteins before encapsidation. Replicated viral genomes accumulate in the central region of the nucleus, which we termed virus-induced postreplication (ViPR) body. However, the molecular mechanism by which the nuclear structure is reorganized and its functional significance in virus production are currently not understood. In this study, we found that viral packaging protein IVa2, but not capsid proteins, accumulated in the ViPR body. In addition, nucleolar chromatin regulatory proteins, nucleophosmin 1 (NPM1), upstream binding factor, and nucleolin accumulated in the ViPR body in late-stage Ad infection. NPM1 depletion increased the nuclease-resistant viral genome and delayed the ViPR body formation. These results suggested that structural changes in the infected cell nucleus depend on the formation of viral chromatin by host chromatin regulatory proteins. Because NPM1 depletion decreases production of the infectious virion, we propose that host factor-mediated viral chromatin remodeling and concomitant ViPR body formation are prerequisites for efficient encapsidation of Ad chromatin.
腺病毒(Ad)基因组被认为通过形成类似于染色质的结构被包装到病毒粒子中。复制的病毒基因组在包装之前可能通过与病毒核心蛋白结合而被浓缩。复制的病毒基因组在核的中央区域积累,我们称之为病毒诱导的复制后(ViPR)体。然而,目前尚不清楚核结构是如何重组的以及它在病毒产生中的功能意义。在这项研究中,我们发现病毒包装蛋白 IVa2 而不是衣壳蛋白在 ViPR 体中积累。此外,核仁染色质调节蛋白核磷蛋白 1(NPM1)、上游结合因子和核仁素在晚期 Ad 感染时在 ViPR 体中积累。NPM1 耗竭增加了核酸酶抗性的病毒基因组并延迟了 ViPR 体的形成。这些结果表明,受感染细胞核的结构变化取决于宿主染色质调节蛋白形成的病毒染色质。由于 NPM1 耗竭会降低感染性病毒粒子的产生,因此我们提出,宿主因子介导的病毒染色质重塑和伴随的 ViPR 体形成是 Ad 染色质有效包装的前提条件。