生物
核运输
细胞生物学
细胞核
染色质
信使核糖核酸
核糖核酸
核出口信号
基因表达
抄写(语言学)
病毒复制
斑点图案
下调和上调
基因沉默
核蛋白
基因
核孔
单纯疱疹病毒
基因表达调控
核定位序列
核基因
病毒学
转录因子
作者
Shani Nadav-Eliyahu,C. Bohrer,Alon Boocholez,Noa Kinor,Vesa Aho,Jennifer I. C. Benichou,Salla Mattola,Sami Salminen,Henri Niskanen,Minna U. Kaikkonen,Maija Vihinen‐Ranta,Y. Shav-Tal
标识
DOI:10.1073/pnas.2511555123
摘要
Herpes simplex virus type 1 (HSV-1) infection remodels the host nucleus, marginalizing chromatin and forming viral replication compartments (VRCs). Nuclear speckles, nuclear bodies enriched in RNA-processing factors, reposition around VRCs and undergo structural changes. While viral mRNAs are transcribed in VRCs and host transcription is largely suppressed, the nuclear routes used by viral and upregulated host transcripts and their relationship with nuclear bodies remain unclear. We show that immediate-early (IE) viral transcripts uniquely accumulate in nuclear speckles prior to export, unlike early or late transcripts, revealing a selective nuclear speckle-dependent pathway. Similarly, host mRNAs upregulated during infection traffic into nuclear speckles after transcription. Moreover, nuclear speckles are structurally remodeled, marked by the long non-coding RNA (lncRNA) MALAT1 removal and increased dynamics of the nuclear speckle core protein SRRM2. Finally, we found that blocking mRNA export causes IE transcripts to accumulate in nuclear speckles and that nuclear speckle disassembly severely impairs IE mRNA export, preventing downstream viral gene expression. These findings establish nuclear speckles as dynamic regulatory hubs that selectively facilitate the processing and export of IE viral mRNAs during HSV-1 infection.
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