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Updated: Jan 28, 2026

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes
Published on: April 13, 2018
Cell Cycle Arrest is a Conserved Function of Norovirus VPg Proteins
Alice McSweeney1, Colin Davies2, Vernon K Ward3
1Department of Microbiology & Immunology, School of Biomedical Sciences, University of Otago, Dunedin 9054, New Zealand. alice.mcsweeney@postgrad.otago.ac.nz.
Murine norovirus (MNV) viral protein genome-linked (VPg) induces a cell cycle arrest for replication. This G0/G1 arrest is conserved across norovirus genogroups and involves the N-terminal region of VPg.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Murine norovirus (MNV) viral protein genome-linked (VPg) manipulates the host cell cycle to promote viral replication.
- The G0/G1 cell cycle arrest induced by MNV VPg is a known mechanism, but its conservation across the norovirus genus was uninvestigated.
Purpose of the Study:
- To determine if the G0/G1 cell cycle arrest function of MNV VPg is conserved in other norovirus genogroups.
- To identify the region of VPg responsible for inducing cell cycle arrest.
Main Methods:
- Transfection of RNA transcripts encoding VPg from five norovirus genogroups into RAW-Blue murine macrophages.
- Analysis of cell cycle phases using flow cytometry.
- Truncation and point mutation analysis of MNV VPg, along with sequence alignment.
Main Results:
- All tested norovirus VPg proteins induced a G0/G1 cell cycle arrest.
- This arrest was also conserved in rabbit hemorrhagic disease virus (RHDV) VPg and human sapovirus (HuSV) VPg.
- The N-terminal 62 amino acids of MNV VPg were sufficient for inducing arrest, and a conserved N-terminal motif was identified.
Conclusions:
- The G0/G1 cell cycle arrest is a conserved function of norovirus VPg proteins.
- The N-terminal region of VPg is crucial for mediating this conserved cell cycle arrest function.
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