Project Title: Identification of cell types underlying genomic evolution in primates and how this relates to genetic risk for brain disorders 
Supervisors:  Dr Nathan Skene, Professor Steve Gentleman, Dr Sarah Marzi 
Location: Sir Michael Uren Hub, White City Campus

About Me

During my undergraduate degree I was fortunate enough to spend a year at the University of Melbourne, where I took the Principles of Neuroscience module. With each lecture being vastly different but just as interesting as the last, I soon realised I would never be bored as a neuroscientist. As a result, I returned to King’s College London and specialised in neuroscience during my final year.

Before graduating I also had the opportunity to complete a year in industry, during which I investigated experimental therapies for sepsis and type 2 diabetes in small animal models at The William Harvey Research Institute in London. After graduating I worked as a research technician in the gut signalling and metabolism lab at LMS, where I investigated the role and regulation of a putative intestinal glucose sensor in murine pregnancy and lactation.

In 2019 I was awarded a 4.5 year MRC DTP Studentship. Having gained experience in the lab, I then wanted to understand how I could apply computational techniques to continue addressing scientific questions. As part of my studentship I completed the MRes in Experimental Neuroscience, during which I undertook three computational projects related to evolution, genomics, and neurodegenerative disease.

I am now a PhD student in the neurogenomics lab. If my head isn’t buried in my laptop, then I’m either cooking or eating.


2020-present: PhD Clinical Medical Research, Imperial College London (expected 2024)

2019-2020: MRes Experimental Neuroscience, Imperial College London

2014-2018: BSc Biomedical Science with extramural year, King’s College London 

Research Interests 

Studying evolutionary pressures on the genome can improve our understanding of human traits and disorders: sequence conservation is currently the best predictor of whether a genetic variant will be associated with human disease. Additionally, both autism and schizophrenia have been linked to genomic loci that have been under selective pressure. I am integrating transcriptomic, epigenomic, and primate genomic data to identify the cell types associated with the evolutionary pressures at key divergence points across primate evolution. Given that genetic risk loci predominantly fall into non-coding and regulatory regions, and changes in regulatory regions have been suggested to account for a greater proportion of adaptive evolution than changes in protein-coding regions, I will extend our modelling to measure selective pressures on regulatory regions. I will also evaluate how this relates to genetic risk for complex brain disorders such as Alzheimer’s disease.

Selected publications

Murphy, KB., Nott, A., Marzi, SJ. CHAS, a deconvolution tool, infers cell type-specific signatures in bulk brain histone acetylation studies of brain disorders. bioRxiv. doi

Collotta, D., Hull, W., Mastrocola, R., Chiazza, F., Cento, A. S., Murphy, C., Verta, R., Alves, G. F., Gaudioso, G., Fava, F., Yaqoob, M., Aragno, M., Tuohy, K., Thiemermann, C., & Collino, M. (2020). Baricitinib counteracts metaflammation, thus protecting against diet-induced metabolic abnormalities in mice. Molecular metabolism39, 101009.

Al Zoubi, S., Chen, J., Murphy, C., Martin, L., Chiazza, F., Collotta, D., Yaqoob, M. M., Collino, M., & Thiemermann, C. (2018). Linagliptin Attenuates the Cardiac Dysfunction Associated With Experimental Sepsis in Mice With Pre-existing Type 2 Diabetes by Inhibiting NF-κB. Frontiers in immunology9, 2996.

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