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. Author manuscript; available in PMC: 2017 Apr 15.
Published in final edited form as: Biol Psychiatry. 2015 Mar 17;79(8):642–649. doi: 10.1016/j.biopsych.2015.03.012

Figure 1.

Figure 1

The use of iPSCs to model ASD has already revealed new biological insights. A recent ASD predisposition gene (TRPC6) was shown to contribute to the formation of glutamatergic synapses in human neurons. Interestingly, TRPC6 gene expression can be controlled by MeCP2, a gene implicated in Rett syndrome, revealing the shared molecular pathways between syndromic and non-syndromic autisms. In non-affected individuals, MeCP2 is part of a currently uncharacterized activator complex in cortical neurons, stimulating the expression of TRPC6 that promotes calcium influx. The downstream activation pathway involves CREB-targets that regulate neuronal homeostasis, including the establishment of excitatory neurons. In a subset of idiopathic ASD individuals, TRPC6 is downregulated due to a reduced level of MeCP2 or mutations in the TRPC6 allele.