ICP22-defined condensates mediate RNAPII deubiquitylation by UL36 and promote HSV-1 transcription

	ICP22-defined condensates mediate RNAPII deubiquitylation by UL36 and promote HSV-1 transcription
	Qi, HS; Yin, MQ; Xiong, F; Ren, XL; Chen, KN; Qin, HB; Wang, ER; Chen, GJ; Yang, LP; Liu, LD; Zhang, H; Cao, X; Fraser, NW; Luo, MH; Zeng, WB; Zhou, JM
	2024
发表期刊	CELL REPORTS
ISSN	2211-1247
卷号	43 期号:10
摘要	Herpes simplex virus type I (HSV-1) infection leads to RNA polymerase II (RNAPII) degradation and host transcription shutdown. We show that ICP22 defines the virus-induced chaperone-enriched (VICE) domain through liquid-liquid phase separation. Condensate-disrupting point mutations of ICP22 increase ubiquitin modification of RNAPII Ser-2P; reduce its level and occupancy on viral genes; impair viral gene expression, particularly late genes; and severely reduce viral titers. When proteasome activity is blocked, ubiquitinated RNAPII Ser-2P and the viral UL36 begin to accumulate in the ICP22 condensates. The ubiquitin-specific protease (USP) deubiquitinase domain of UL36 interacts with and erases ubiquitin modification from RNAPII Ser-2P, protecting it from degradation in infected cells. A virus carrying a catalytic mutant of the UL36 USP diminishes cellular RNAPII Ser-2P levels, viral transcription, and growth. Thus, ICP22 condensates are processing centers where RNAPII Ser-2P is recruited to be deubiquitinated to ensure viral transcription when host transcription is disrupted following infection.
收录类别	SCI
语种	英语
文献类型	期刊论文
条目标识符	http://ir.kiz.ac.cn/handle/152453/14576
专题	科研部门_基因调控与表达遗传（周巨民）
推荐引用方式 GB/T 7714	Qi, HS,Yin, MQ,Xiong, F,et al. ICP22-defined condensates mediate RNAPII deubiquitylation by UL36 and promote HSV-1 transcription[J]. CELL REPORTS,2024,43(10).
APA	Qi, HS.,Yin, MQ.,Xiong, F.,Ren, XL.,Chen, KN.,...&Zhou, JM.(2024).ICP22-defined condensates mediate RNAPII deubiquitylation by UL36 and promote HSV-1 transcription.CELL REPORTS,43(10).
MLA	Qi, HS,et al."ICP22-defined condensates mediate RNAPII deubiquitylation by UL36 and promote HSV-1 transcription".CELL REPORTS 43.10(2024).

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