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CRISPR介导的pp38/pp24基因激活(CRISPRa)调控引发马立克氏病病毒转化细胞系裂解感染的事件。

CRISPR-Mediated Gene Activation (CRISPRa) of pp38/pp24 Orchestrates Events Triggering Lytic Infection in Marek's Disease Virus-Transformed Cell Lines.

作者信息

Roy Poornima, Moffat Katy, Nair Venugopal, Yao Yongxiu

机构信息

Viral Oncogenesis Group, The Pirbright Institute, Pirbright, Surrey GU24 0NF, UK.

The Jenner Institute Laboratories, University of Oxford, Oxford OX3 7DQ, UK.

出版信息

Microorganisms. 2021 Aug 8;9(8):1681. doi: 10.3390/microorganisms9081681.

Abstract

Marek's disease (MD) is an immunosuppressive and highly contagious lymphoproliferative disease caused by Marek's disease virus (MDV) in poultry. Lymphoblastoid cell lines (LCLs) generated ex vivo from MD lymphomas are considered excellent models to study virus-host molecular interactions. LCLs mostly have latently infected MDV genome, but many of them also have varying populations of lytically-infected cells, thus making them very suitable to examine the molecular events associated with the switch from latent to lytic infection. MDV-encoded phosphoprotein 38 (pp38) is readily detectable in lytically-infected LCLs and hence considered as a biomarker for lytic infection. Whilst previous studies have suggested that pp38 is essential for the early cytolytic infection of B-cells, its role in the switch from latent to lytic infection of LCLs is still unclear. pp24, another phosphorylated protein in the same protein complex, shares the same promoter and N-terminal 65 amino acids as pp38. In this study we employed CRISPR activation (CRISPRa) technology for targeted activation of pp38/pp24 in LCLs to investigate their role in inducing lytic infection. Our results show that enforced expression of pp38/pp24 through CRISPRa induces orchestrated upregulation of other MDV genes including ICP4, gB, Meq and pp14 as well as differential expression of host genes thereby facilitating lytic infection. Our results also show that pp38/pp24 expression induces the lytic switch through inhibiting apoptosis.

摘要

马立克氏病(MD)是由家禽马立克氏病病毒(MDV)引起的一种免疫抑制性且高度传染性的淋巴细胞增生性疾病。从MD淋巴瘤体外生成的淋巴母细胞样细胞系(LCLs)被认为是研究病毒-宿主分子相互作用的优秀模型。LCLs大多潜伏感染MDV基因组,但其中许多也有不同数量的裂解感染细胞,因此使其非常适合研究与从潜伏感染转变为裂解感染相关的分子事件。MDV编码的磷蛋白38(pp38)在裂解感染的LCLs中易于检测到,因此被视为裂解感染的生物标志物。虽然先前的研究表明pp38对于B细胞的早期细胞溶解感染至关重要,但其在LCLs从潜伏感染转变为裂解感染中的作用仍不清楚。pp24是同一蛋白复合物中的另一种磷酸化蛋白,与pp38共享相同的启动子和N端65个氨基酸。在本研究中,我们采用CRISPR激活(CRISPRa)技术在LCLs中靶向激活pp38/pp24,以研究它们在诱导裂解感染中的作用。我们的结果表明,通过CRISPRa强制表达pp38/pp24会诱导包括ICP4、gB、Meq和pp14在内的其他MDV基因的协调上调以及宿主基因的差异表达,从而促进裂解感染。我们的结果还表明,pp38/pp24表达通过抑制细胞凋亡诱导裂解开关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b6ef/8398467/c257e8adb29a/microorganisms-09-01681-g001.jpg

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