Dr Elaine TaylorDirector of Student Support & Lecturer in Medical Sciences
My research interests are in understanding how cells normally function to prevent, or reverse, deleterious genetic alterations and chromosomal abnormalities. Such loss of genome integrity can lead to a range of disorders including cancer and neurodegeneration. Ubiquitin and SUMO modification of specific proteins is recognised as an important element of the cellular response to genetic damage. A key focus of my research is to identify and characterise Ub/SUMO modification targets involved in genetic maintenance through a combination of biochemical and cell biological approaches. In doing so, we aim to uncover novel targets for future drug discovery.
Projects available in my laboratory include:-
- Analysis of ubiquitin modification in response to DNA damage and replication stress
- Analysis of SUMO modification in response to DNA damage and replication stress
- The regulation of chromosome replication and segregation
All cells must ensure that their chromosomes are copied and segregated accurately during cell division and that any damage to their genetic material is repaired. Failure to do so will result in the sort of genetic alterations that lie behind disorders such as cancer, neurodegeneration and even ageing. Determining how cells normally act to maintain genome integrity, and identifying defects in these genome maintenance mechanisms in individual disease states, is therefore vital to our understanding of how disease develops and for identifying new possibilities for intervention and treatment.
Cells possess a complex network of DNA damage response (DDR) pathways that can detect problems with genome integrity and initiate a series of responses, such as DNA repair, arrest of cell cycle progression until the problem is rectified or, if the problem is too great, programmed cell death. Much of the signalling involved in DDR pathways relies on post-translational modification of cellular proteins to trigger changes in their behaviour. Protein phosphorylation events play a key role within many DDR pathways and have been the subject of intense study. More recently it has become clear that other post-translational changes, such as ubiquitylation and sumoylation, are also vitally important in genome maintenance.
My research interests are in understanding how cells maintain genome integrity and, in particular, in understanding the role played by ubiquitin and SUMO modification in this process. Through a combination of biochemical analysis, using purified proteins and cell-free extracts of Xenopus laevis eggs, and in vivo cell biological analysis using established human cell lines, my group is identifying key targets of ubiquitin and SUMO modification in the DNA damage response.
Currently I teach the following modules:
- MEDI101: Lecturer in Medical Sciences and Problem-Based Learning Facilitator
- MEDI106: Special Study Module Convenor for studies in relation to genome instability and human health
- BIOL386 Bioscience Research Project: Projects on DNA damage responses and cell cycle control
- BIOL466 Masters Research Project: Projects on DNA damage responses and cell cycle control
I am the Director of Student Support for Lancaster Medical School. In this capacity I provide, co-ordinate and monitor both pastoral and academic support for students from all five years of study within the medical degree (MBChB) programme.
PhD Supervision Interests
Please contact me if you are interested in doing a PhD in the area of genome stability and DNA repair. Details of specific projects available in my research group can usually be found on FindaPhd.com. Applications for self-funded study can be made at any time.
Selected Publications Show all 20 publications
Molecular basis for PrimPol recruitment to replication forks by RPA
Guilliam, T.A., Brissett, N.C., Ehlinger, A., Keen, B.A., Kolesar, P., Taylor, E.M., Bailey, L., Lindsay, H.D., Chazin, W.J., Doherty, A.J. 23/05/2017 In: Nature Communications. 8, 14 p.
DNA replication stress and cancer: cause or cure?
Taylor, E.M., Lindsay, H.D. 01/2016 In: Future Oncology. 12, 2, p. 221-237. 17 p.
PrimPol bypasses UV photoproducts during chromosomal DNA replication
Bianchi, J., Rudd, S.G., Jozwiakowski, S.K., Bailey, L.J., Soura, V., Taylor, E., Stevanovic, I., Green, A.J., Stracker, T.H., Lindsay, H., Doherty, A.J. 21/11/2013 In: Molecular Cell. 52, 4, p. 566-573. 8 p.
SMC6 is an essential gene in mice, but a hypomorphic mutant in the ATPase domain has a mild phenotype with a range of subtle abnormalities
Ju, L., Wing, J., Taylor, E., Brandt, R., Slijepcevic, P., Horsch, M., Rathkolb, B., Racz, I., Becker, L., Hans, W., Adler, T., Beckers, J., Rozman, J., Klingenspor, M., Wolf, E., Zimmer, A., Klopstock, T., Busch, D., Gailus-Durner, V., Fuchs, H., Hrabe de Angelis, M., van der Horst, G., Lehmann, A. 1/05/2013 In: DNA Repair. 12, 5, p. 356-366. 11 p.
Depletion of Uhrf1 inhibits chromosomal DNA replication in Xenopus egg extracts
Taylor, E., Bonsu-Dartnall, N., Price, J., Lindsay, H. 20/06/2013 In: Nucleic Acids Research. 41, 16, p. 7725-7737. 13 p.
The Mre11/Rad50/Nbs1 complex functions in resection-based DNA end joining in Xenopus laevis.
Taylor, E.M., Cecillon, S.M., Bonis, A., Chapman, J.R., Povirk, L.F., Lindsay, H.D. 01/2010 In: Nucleic Acids Research. 38, 2, p. 441-454. 14 p.
Identification of the proteins, including MAGE-G1, that make up the human SMC5-6 protein complex.
Taylor, E.M., Copsey, A., Hudson, J., Vidot, S., Lehmann, A. 15/02/2008 In: Molecular and Cellular Biology. 28, 4, p. 1197-1206. 10 p.
Composition and architecture of the Schizosaccharomyces pombe Rad18 (Smc5-6) complex.
Sergeant, J., Taylor, E., Palecek, J., Fousteri, M., Andrews, E., Sweeney, S., Shinagawa, H., Watts, F. 01/2005 In: Molecular and Cellular Biology. 25, 1, p. 172-184. 13 p.
Nse2, a component of the Smc5-6 complex, is a SUMO ligase required for the response to DNA damage.
Andrews, E., Palecek, J., Sergeant, J., Taylor, E., Lehmann, A., Watts, F. 01/2005 In: Molecular and Cellular Biology. 25, 1, p. 185-196. 12 p.