Martin Taylor Research Group

Research in a Nutshell 

We study why mutations occur where they do and what effect they have when they arise. Genetic mutations are important, they are responsible for inherited disease, drive the development of cancer, allow bacteria and viruses to escape our drugs and immune system, and provide the raw material for evolution. Most of our research spans our three core aims:

1. Understanding mutational processes. What processes go wrong in our cells to create mutations and how damage to our DNA contributes to this. We are especially interested in the mutations that get inherited from one generation to the next, and those that drive the progression to cancer.

2. Interpreting genetic variation. Revealing which mutations have an important biological effect and which are less important. This helps genetic diagnosis and matching the cancer treatment to the patient. We are increasingly realising that combinations of mutations are important for how cells grow and the development of cancer.    

3. Learning how mutations alter the regulation of our genes. As a community we can work out fairly well when a mutation is likely to alter the function of a protein, we’ve still got a lot to learn about how mutations alter the production of a protein from a gene. Studying the changes through past evolution helps us understand the effect of new mutations of gene regulation.

1. Anderson CJ, Talmane L, Luft J, Connelly J, Nicholson MD, Verburg JC, Pich O, Campbell S, Giaisi M, Wei PC, Sundaram V, Connor F, Ginno PA, Sasaki T, Gilbert DM; Liver Cancer Evolution Consortium; López-Bigas N, Semple CA ,Odom DT, Aitken SJ, Taylor MS. Strand-resolved mutagenicity of DNA damage and repair. Nature 2024. doi.org/10.1038/s41586-024-07490-1
2. Nicholson MD, Anderson CJ, Odom DT, Aitken SJ, Taylor MS. DNA lesion bypass and the stochastic dynamics of transcription-coupled repair. PNAS. 2024 121 (20) e2403871121. doi/10.1073/pnas.2403871121
3. Ginno PA, Borgers H, Ernst C, Schneider A, Behm M, Aitken SJ, Taylor MS, Odom DT. Single-mitosis dissection of acute and chronic DNA mutagenesis and repair. Nature Genetics. 2024 doi.org/10.1038/s41588-024-01712-y
4. Reijns MAM, Parry DA, Williams TC, Nadeu F, Hindshaw RL, Rios Szwed DO, Nicholson MD, Carroll P, Boyle S, Royo R, Cornish AJ, Xiang H, Ridout K, Schuh A, Aden K, Palles C, Campo E, Stankovic T, Taylor MS, Jackson AP. Signatures of TOP1 transcription-associated mutagenesis in cancer and germline. Nature. 2022; 1–9. doi:10.1038/s41586-022-04403-y
5. Aitken SJ, Anderson CJ, Connor F, Pich O, Sundaram V, Feig C, Rayner TF, Lukk M, Aitken S, Luft J, Kentepozidou E, Arnedo-Pac C, Beentjes SV, Davies SE, Drews RM, Ewing A, Kaiser VB, Khamseh A, López-Arribillaga E, Redmond AM, Santoyo-Lopez J, Sentís I, Talmane L, Yates AD, Liver Cancer Evolution Consortium, Semple CA, López-Bigas N, Flicek P, Odom DT, Taylor MS. Pervasive lesion segregation shapes cancer genome evolution. Nature. 2020;583: 265–270. doi:10.1038/s41586-020-2435-1
6. Reijns MAM, Kemp H, Ding J, de Procé SM, Jackson AP, Taylor MS. Lagging-strand replication shapes the mutational landscape of the genome. Nature. 2015;518: 502–506. doi:10.1038/nature14183

Full publication list can be found on Research Explorer: Martin Taylor — University of Edinburgh Research Explorer

• Dr Sarah Aitken, Yale University, US.
• Dr Luke Boulter, IGC, Edinburgh, UK
• Professor Javier Caceres, IGC, Edinburgh, UK
• Professor Giulio Caravagna, University of Trieste, Italy
• Professor Paul Flicek, The Jackson Laboratory, US.
• Dr Anton Gartner, Institute for Basic Science, South Korea
• Professor Andrew Jackson, IGC, Edinburgh, UK
• Dr Ava Khamseh, IGC & Informatics, Edinburgh, UK
• Professor Núria López-Bigas, IRB, Barcelona, Spain
• Dr Michael Nicholson, School of Mathematics, Edinburgh, UK
• Professor Duncan Odom, DKFZ, Heidelberg, Germany.
• Professor Liz Patton, IGC, Edinburgh, UK
• Professor Colin Semple, IGC, Edinburgh, UK

• MRC
• FANTOM Consortium
• Scottish Genomes Partnership