Jo is interested in supervising doctoral research students in the following areas:
The study of novel HPV-host interactions important for the control of viral gene expression and completion of the viral life cycle.
The study of HPV-virus interactions important for the maintenance of persistent HPV infections.
If you are interested in studying any of these subject areas please contact Jo, or for any general doctoral research enquiries, please email: firstname.lastname@example.org or call +44 (0)121 414 5005.
For a full list of available Doctoral Research opportunities, please visit our Doctoral Research Programme listings.
Jo’s research group is focused on the cellular pathways involved in maintaining host cell genome stability and long-term human papillomavirus (HPV) persistence.
HPV infection is associated with the development of benign lesions or warts, and several malignant lesions of the epidermal layer including cervical cancer. The majority of sexually active adults will become infected with a genital HPV type at least once in their lives, which can result in persistent, disfiguring and hard to treat genital warts or in the development of carcinoma, particularly in patients that maintain a latent ‘high-risk’ infection over many years. Although HPV infection causes carcinoma in a relatively small number of infected individuals, 99.7% of cervical carcinomas are associated with HPV infection and each year 240,000 cervical cancer related deaths are reported.
To complete their life cycle, all viruses must synthesise proteins in an ordered and concerted manner, copy their genomes (DNA), and partition genomes to new cells during cell division. This ensures long term or latent infection.
Work in the Parish laboratory is primarily focused on how HPV genomes are passed to daughter cells during mitotic division. To ensure the passage of viral genomes to new cells, papillomaviruses hijack some of the mechanisms that exist in host cells required the maintenance of genome stability. In particular, the HPV E2 protein targets several cellular proteins during DNA replication and mitosis to facilitate attachment of genomes to mitotic chromosomes. Work is on going to characterise these virus-host interactions and the cellular pathways hijacked by HPV and decipher their importance in the HPV life cycle.
Feeney K. M., McFarlane-Majeed L., and Parish J.L. Analyzing sister chromatid cohesion in mammalian cells. In: Noguchi E., and Gadaleta M. ed. Cell Cycle Control: Mechanisms and Protocols, Second Edition. Methods in Molecular Biology, Humana Press/Springer. In Press
Prystowsky M. B., Feeney K. M., Kawachi N., Montagne C., Willmott M. K. S., Wasson C. W., Antkowiak M., Loudig O. and Parish J. L. (2013) Inhibition of Plk1 and Cyclin B1 expression results in panobinostat-induced G2 delay and mitotic defects. Scientific Reports. 3:2640. DOI: 10.1038/srep02640
Feeney K. M., Saade A., Okrasa K. and Parish J. L., (2011) In vivo analysis of the cell cycle dependent association of the bovine papillomavirus E2 protein and ChlR1. Virology. 414:1-9.
Feeney K. M, Wasson C. and Parish J. L., (2010) Cohesin: Regulator of Genome Integrity and Gene Expression. Biochemical Journal. 428 (2):147-159.
Jolly C. E., Gray L. J., Parish J. L., Lain S. and Herrington C. S., (2009), Leptomycin B Induces Apoptosis in Cells Containing the Whole HPV 16 Genome. The International Journal of Oncology. 35:649-656.
Prystowsky M. B., Adomako A., Smith R. V., Kawachi N., McKimpson W., Atadja P., Chen Q., Schlecht N., Parish J. L., Childs G. and Belbin T., (2009), The histone deacetylase inhibitor LBH589 inhibits expression of mitotic genes causing G2/M arrest and cell death in head and neck squamous cell carcinoma cell lines. Journal of Pathology. 218 (4):467-477.
Feeney K.M. and Parish J. L., (2009), Targeting mitotic chromosomes: a conserved mechanism to ensure viral genome persistence. Proceedings of the Royal Society B: Biological Sciences. 276 (1662):1535-44.
Parish J. L., Bean A.M., Park R.B., Androphy E.J., (2006), ChlR1 is required for loading papillomavirus E2 onto mitotic chromosomes and viral genome maintenance. Molecular Cell. 24(6), 70-76.
Parish J. L., Rosa J., Wang X., Lahti J., Doxsey S. J., Androphy E. J., (2006), The DNA helicase ChlR1 is required for sister chromatid cohesion in mammalian cells. Journal of Cell Science. 119, 4857-4865.
Parish J. L., Kowalczyk A., Chen H-T., Roeder G., Sessions R., Buckle M. and Gaston K., (2006), The E2 proteins from high- and low-risk HPV type differ in their ability to bind p53 and induce apoptotic cell death. Journal of Virology. 80 (9), 4580-90.