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Murine cytomegalovirus evolved a cell cycle regulator (m54.5) within the highly conserved viral DNA polymerase gene

ABSTRACT: Systems biology approaches have revealed a surprising complexity of herpesvirus gene products. Using advanced sequencing approaches, we discovered a novel gene, m54.5, encoded within a highly conserved region of the murine cytomegalovirus (MCMV) genome. This gene produces a nuclear protein, m54.5p, abundantly expressed early during infection. We show that m54.5p interacts with host cell cycle regulators—the anaphase-promoting complex/cyclosome (APC/C) and phosphatase-6 (PP6)—to arrest cells in G1 phase and block progression into S phase. This function and underlying mechanism is reminiscent of the unrelated UL21a protein in human cytomegalovirus, illustrating how distinct viruses can evolve similar strategies to control host cell division. Despite its role in cell cycle disruption, m54.5p is not required for MCMV replication in cultured cells, suggesting redundant viral mechanisms. Our findings reveal the unexpected plasticity of herpesvirus genomes to evolve new, functional transcripts and proteins even within the most highly conserved genomic regions. Our findings thereby reshape our understanding of herpesvirus evolution and virus-host interaction.

INSTRUMENT(S):

ORGANISM(S): Murine Cytomegalovirus (strain Smith) Mus Musculus (mouse)

TISSUE(S): Cell Culture, Fibroblast

SUBMITTER: Yan Zheng

LAB HEAD: Lars Dölken

PROVIDER: PXD066167 | Pride | 2026-05-16

REPOSITORIES: Pride

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			Action	DRS
	2022-05-05-_Fusion_31706.raw	Raw
	2022-05-05-_Fusion_31707.raw	Raw
	2022-05-05-_Fusion_31708.raw	Raw
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	2022-05-05-_Fusion_31710.raw	Raw

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Project description:Porcine cytomegalovirus (PCMV) is a member of the genus Cytomegalovirus, subfamily Betaherpesvirinae, and family Herpesvirus. PCMV is a major immunosuppressive virus that mainly suppress the immune function of T lymphocytes and macrophages. PCMV is widely distributed all over the world, but there are not significantly different serotypes found. Moreover, the molecular mechanisms of host anti-PCMV infection and the molecular immunosuppressive mechanisms of PCMV is still not well charaterized. To understand the PCMV potential impact on the function of immune organs, we performed microarray assay to analyze the transcriptome of porcine immune organs after PCMV infection. We identified 5582 differential expression genes by PCMV infection in microarray. There are 2161 upregulated genes and 3421 down-regulated by PCMV infection genes compare to the uninfected control group. We confirmed 13 differentially expressed immune-related genes by quantitative real-time RT-PCR (qPCR). Gene ontology, gene interaction networks and KEGG pathway analysis uncovered the differentially expressed genes interaction regulatory network. These findings indicated that PCMV regulates multiple functional pathways, including immune system process, cellular process, metabolic process, networks of cytokine-cytokine receptor interaction, TGF-beta signaling pathway, lymphocytes receptor signaling pathway and TNF signaling pathway. Our study is the first comprehensive attempt to explore the host transcriptional response to PCMV infection in porcine immune systems. It provided new insights into the immunosuppressive molecular mechanisms and pathogenesis of PCMV. This previously unrecognized endogenous antiviral mechanism has implications for development of host-directed strategies to the prevention and treatment of immunosuppressive viral diseases. 2 samples were analysed. PCMV infected porcine immune organs; control porcine organs. piglets were divided into two groups of five pigs each, and maintained under controlled temperature and humidity. Each pig in the first group was inoculated with 5 ml of 109 PFU/ml PCMV SC strain by intramuscular and intranasal injection, and the other five pigs were injected with 5 ml of RPMI-1640 nutrient solution (Thermo Fisher Scientific, Waltham, UK) as the control. The sera, lymph nodes, spleens, and thymuses of the infected and control pigs were collected at 14 dpi

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Murine cytomegalovirus evolved a cell cycle regulator (m54.5) within the highly conserved viral DNA polymerase gene

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