The genetics of autism has proven to be as complex as the genetics of other diseases in people. As seen in many human diseases, candidate genes appear to affect a wide range of biological processes, but not very consistently.

Ralph Greenspan and his colleagues at the University of California, San Diego hypothesized that the disparate nature of these processes indicates a wide-ranging, interacting network of genes capable of influencing autism. Greenspan and his group set out to map this network in the fruit fly, where it can most easily be done, with the eventual goal of confirming and expanding the network in mammals, and ultimately applying the findings to humans. The genetic similarities between flies and humans are extensive, even for genes affecting cognitive disability in humans.

The strategy was to construct strains of Drosophila fruit flies carrying mutations in each of seven genes that have been associated with autism, and test for those genes’ effects on social behavior and on the regulation of other genes.

Several of the tested autism gene homologs were found to affect fly social behavior and also other genes’ expression levels. This suggests that there is a common network, or more than one common network, susceptible to autism predisposition when affected by mutations. It will be important to explore this possibility further in an effort to understand the most accessible points in the system for potential intervention in the treatment of autism.

Understanding the network relationships among the many disparate genes associated with autism has the potential to offer uniquely powerful strategies for treatment, and possibly even prevention, of the underlying causes of the disorder.