John Perry

To explore this, we use large-scale human population studies to identify genetic variants that influence risk of disease or contribute to variation in quantitative traits. Through integration with transcriptomic and proteomic datasets we can then prioritise genes and pathways for evaluation with experimental collaborators using animal and cellular models.

My research is primarily based within the Institute of Metabolic Science where I co-lead an MRC-funded programme with Professor Ken Ong. My Associate position at the Gurdon Institute focusses on one of the key biological mechanisms emerging from our population-based research: DNA damage response (DDR).

Although often considered in the context of cancer susceptibility, it is now clear that DDR processes influence other complex diseases and traits. For example, our human genetics work has highlighted DDR as the major pathway governing reproductive ageing and fertility in women. We aim to better understand these processes, when they act over the life-course and how they might be modified to preserve fertility and prevent disease.

Overview of process to identify disease- and trait-associated alleles, genes and biological pathways using large-scale human population studies. Genetic variation is measured genome-wide in populations of research participants. Individual genetic variants associated with diseases and traits can then be identified through computational approaches, linked to gene function through the integration of ‘omics’ resources and further evaluated in downstream experimental models.