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Modulation of the cell division cycle by human papillomavirus type 18 E4
Tomomi Nakahara1, Akiko Nishimura, Masakazu Tanaka
1Laboratory of Gene Analysis, Department of Viral Oncology, Institute for Virus Research, Kyoto University, Sakyo-Ku, Kyoto 606-8507, Japan.
Journal of Virology
|October 9, 2002
Summary
Human papillomaviruses (HPVs) E4 protein expression halts cell division at the G(2)/M phase, impacting virus replication. This growth arrest function is mediated by the central E4 region and is separate from its effect on cytokeratin filaments.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- Human papillomaviruses (HPVs) life cycle is linked to epithelial cell differentiation.
- HPV E4 gene expression occurs in parabasal layers, suggesting a role in differentiation-dependent replication.
- The precise biological function of HPV E4 protein remains largely unknown.
Purpose of the Study:
- To investigate the effect of HPV type 18 E4 on host cell proliferation.
- To identify the functional domain of E4 responsible for modulating cell growth.
Main Methods:
- Analysis of HPV type 18 E4 expression in epithelial cells.
- Cell cycle progression assays to evaluate proliferation.
- Mapping of the E4 functional region for growth arrest activity.
Main Results:
- HPV type 18 E4 expression induced cell cycle arrest at the G(2)/M phase.
- The central region of the E4 protein was identified as essential for growth arrest activity.
- This growth arrest activity was independent of E4-induced disruption of cytokeratin intermediate filaments.
Conclusions:
- HPV E4 protein plays a role in regulating host cell proliferation.
- The G(2)/M cell cycle arrest mediated by E4 may influence HPV replication strategies.
- Understanding E4's function provides insights into HPV pathogenesis and viral replication mechanisms.