What regulates human behaviour and how?

Genomics data has recently revealed causal relationships between specific genetic variation and risk for neuropsychiatric disease. However, there still remains a missing link tying genetic variation to changes at the molecular, cellular, and systems biology and behaviour levels. This is due, in part, to (1) the lack of integration of molecular and cellular biology, electrophysiology, behaviour and neuroanatomical data, and (2) the lack of high fidelity model systems that can be used to experimentally validate genetic/epigenetic effects.

Our goal is to provide this "missing" link by using both high-throughput methodologies and experimental validation of their predictions in order to clarify how behavioural patterns are affected by genetic and environmental backgrounds, and how a human brain creates risks for mental illness during its development.

Our Projects

The notion that Contactins (CNTNs) are implicated in Neuropsychiatric disorders, resides in findings in genetic studies on sporadic and syndromic cases of ASD. Bipolar disorder with alcohol dependence and other comorbidities was associated with SNP located in the region between the CNTN4 and CNTN6 gene (Kerner et al., 2011). CNVs disrupting the CNTN6/CNTN4/CHL1 region on chromosome 3 have been found in several anorexia nervosa cases. These results strongly suggest that disruption of CNTN4 renders individuals prone to these neuropsychiatric disorders, involving an unknown common mechanism.

Here we work a fundamentally based integrative approach for functional analysis of multi-psychiatric disorder target gene, Contactin4 (CNTN4) and 3p deletion, using in vivo and in vitro models.

We are working with Complex Disease Epigenetics Group ( and Axonology group (