小鼠多瘤病毒感染诱导片层重组

Kateřina Bruštíková, Boris Ryabchenko, Sandra Žáčková, Vojtěch Šroller, Jitka Forstová, Lenka Horníková
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引用次数: 0

摘要

核薄层是核内膜下由中间丝组成的致密网络。核薄层由A型薄片(薄片A/C)和B型薄片(薄片B1和B2)组成,为核膜和染色质提供支架,从而保持细胞核结构的完整性。A型片层蛋白也存在于细胞核内,它们与染色质相互作用,参与基因调控。在细胞核内复制的病毒必须在感染初期和病毒后代的核排出过程中克服核包膜。在这里,我们重点研究了片层蛋白在dsDNA病毒--小鼠多瘤病毒--复制周期中的作用。在小鼠多瘤病毒感染的晚期阶段,我们检测到主要的囊膜蛋白VP1在核外围聚集、核薄层染色缺陷和不同的片层蛋白A/C磷酸化模式,但核膜仍然完好无损。片层蛋白 A/C的缺失不会影响复制复合物的形成,但会减缓病毒的传播。根据我们的研究结果,我们认为核膜是复制复合物形成的支架,而片层 A/C在小鼠多瘤病毒感染的早期阶段起着至关重要的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Mouse polyomavirus infection induces lamin reorganisation
The nuclear lamina is a dense network of intermediate filaments beneath the inner nuclear membrane. Composed of A‐type lamins (lamin A/C) and B‐type lamins (lamins B1 and B2), the nuclear lamina provides a scaffold for the nuclear envelope and chromatin, thereby maintaining the structural integrity of the nucleus. A‐type lamins are also found inside the nucleus where they interact with chromatin and participate in gene regulation. Viruses replicating in the cell nucleus have to overcome the nuclear envelope during the initial phase of infection and during the nuclear egress of viral progeny. Here, we focused on the role of lamins in the replication cycle of a dsDNA virus, mouse polyomavirus. We detected accumulation of the major capsid protein VP1 at the nuclear periphery, defects in nuclear lamina staining and different lamin A/C phosphorylation patterns in the late phase of mouse polyomavirus infection, but the nuclear envelope remained intact. An absence of lamin A/C did not affect the formation of replication complexes but did slow virus propagation. Based on our findings, we propose that the nuclear lamina is a scaffold for replication complex formation and that lamin A/C has a crucial role in the early phases of infection with mouse polyomavirus.
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