Speaker

Jonathan Flint has been a pioneer in the genetics of behaviour. He showed that behaviour, and psychiatric diseases are genetically tractable targets, and he has made key advances in identifying their molecular underpinnings, particularly with his work on structural variants.   His genome-wide analyses of behaviour in rodents, precursors to GWAS in humans, revealed the polygenic architecture of behavior, arising from the joint action of many loci of small effect, a key insight for the design and interpretation of genetic studies in psychiatry.

His work has had clinical relevance: probes developed in his laboratory are now part of standard screening protocols for intellectual disability across the world; his work on determining the causal pathway from mutation to behavioural phenotype resulted in the discovery of an important and unexpected cause of a human genetic disorder (neuronal migration defects), again with benefits for patients and families.

He developed and pioneered novel approaches in mouse genetics, championing the use of multi-parental lines and outbred mice. Together with the widely used sequence data of classical inbred strains, these ideas and resources have transformed complex trait analysis in rodents.

His insistence on the importance of careful delineation of phenotypes in psychiatric genetics resulted in his successful genetic analysis of major depression, and has opened new avenues to understanding the origins of the world’s leading cause of disability. Such work is necessary to develop new ways of treating patients.

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