Autistic individuals have impaired communication and social behaviour. Genes operating across a wide range of different biological functions have been identified as being associated with an increased risk of autism.
However, it is currently unclear how variation in a number of these genes brings about changes in signalling to disrupt the output of neural circuits.
We have developed a pipeline using the model organism C. elegans to identify genes that function to co-ordinate social behaviour. Of these, a subset function within epigenetic and lipid signalling pathways and represent interesting targets for the development of therapeutic approaches.
The student will extend the existing pipeline by using molecular genetic approaches, such as CRISPR, in C. elegans and mammalian neurons to introduce genetic variation identified from human cohorts and develop knowledge of the molecular, cellular and circuit level affects.
For full details please click here.
General enquiries should be made to James Dillon at jcd(atsoton.ac.uk. Any queries on the application process should be made to fels-pgr-apply(T)soton.ac.uk
