New Insights Into Autism From the Candidate Genes-Centered Interactome

Friday, May 18, 2012: 11:30 AM
Grand Ballroom East (Sheraton Centre Toronto)
10:15 AM
R. Corominas1, X. Yang2,3, G. N. Lin1, S. Kang4, Y. Shen2,3, S. A. Wanamaker2,3, S. Tam2,3, M. Rodriguez2,3, M. Broly2,3, J. Sebat4, K. Salehi-Ashtiani2,3, D. E. Hill2,3, M. Vidal2,3, T. Hao2,3 and L. M. Iakoucheva1, (1)Department of Psychiatry, University of California San Diego, La Jolla, CA, (2)Center for Cancer Systems Biology (CCSB) and Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA, (3)Department of Genetics, Harvard Medical School, Boston, MA, (4)Psychiatry, University of California San Diego, San Diego, CA
Background:  Autism is a neurodevelopmental disorder with strong genetic basis. The number of genes that have now been firmly established as strong risk factors for autism is large, and these genes are functionally heterogeneous. Hence, it is important to understand how these multiple genes and their protein product interact within the context of cellular pathways.

Objectives: We have investigated autism from a systems biology perspective with the aim of defining protein interaction networks/pathways/functional modules that connect this diverse set of genes. 

Methods:  Our integrative approach consisted of (1) cloning autism candidate genes from normal adult and fetal brain RNA; (2) Screening these genes against the hORFeome (~15,000 clones) by yeast-two-hybrid (Y2H) experiments to detect protein-protein interactions; (3) building interactome of autism candidate genes; (4) interactome  analysis to define key functional modules.

Results:  (a) We selected 191 autism candidate genes and successfully cloned 124. We added 45 clones from the hORFeome collection; (b) We performed Y2H for 169 genes and detected interactions between 75 autism candidate genes and 272 human proteins that were retested positively four times; (c) We have constructed autism interactome with 492 unique interactions; (d) 93% of the detected interactions are novel and have not been previously reported in the public databases.

Conclusions:  (a) We have detected interaction partners (preys) that are shared between autism candidate genes, thereby implicating new gene targets in autism; (b) We have detected new interactions between well-known autism candidate genes; (c) We have identified preys that connect genes from different autism CNVs on a protein level; (d) Autism network is enriched in preys with autism CNV membership;  (e) Autism network is significantly enriched in co-expressed genes; (f) Autism network is enriched in differentially expressed genes, specifically in down-regulated genes.

Our new autism interactome represents a valuable resource for the research community and for future autism studies.

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