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Expression of human papillomavirus 16 E2 protein in Schizosaccharomyces pombe delays the initiation of mitosis

Oncogene volume 18, pages 4015–4021 (1999)Cite this article

Abstract

Infection by some types of human papillomavirus (HPV) is associated with the development of cervical cancer. Analysis of viral DNA from cervical tumours shows that the E2 gene is frequently disrupted during integration into the host cell's DNA. It has therefore been suggested that loss of E2p is an important step in malignant transformation. Expression of E2p in the fission yeast Schizosaccharomyces pombe retards the G2-M transition, by delaying activation of Cdc2p kinase. In contrast, S phase progression, and commitment to cell division in late G1 are not affected. The delay is independent of the transcriptional trans-activation function of E2p, and does not result from E2p DNA binding mimicking DNA damage. Increased expression of E2p also delays mitotic initiation in mammalian cells. S. pombe may thus provide a simple model for the analysis of E2p function.

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Acknowledgements

Thanks are due to Susanne Schmidt, Deborah Poloni, Lorenzo Cerutti, Marc Sohrmann, Nicola Beltraminelli and Xavier LeGoff, for helpful discussions and advice. We thank Beatrice Bentele, Elena Cano and Nicole Paduwat for technical assistance. This work was funded by the Swiss Cancer League, the Swiss National Science Foundation, ISREC, and the Roche Research Foundation.

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Authors and Affiliations

  1. Virology Department, Swiss Institute for Experimental Cancer Research, Epalinges, 1066, Switzerland

    Nadine Fournier, Kenneth Raj, Philippe Saudan & Peter Beard

  2. Cell Cycle Control Laboratory, Swiss Institute for Experimental Cancer Research, Epalinges, 1066, Switzerland

    Suzan Utzig & Viesturs Simanis

  3. Microbiology Department, CHUV, Lausanne, 1011, Switzerland

    Roland Sahli

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  1. Nadine Fournier
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Fournier, N., Raj, K., Saudan, P. et al. Expression of human papillomavirus 16 E2 protein in Schizosaccharomyces pombe delays the initiation of mitosis. Oncogene 18, 4015–4021 (1999). https://doi.org/10.1038/sj.onc.1202775

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