T-Brain-1 (TBR1), a causative gene in autism spectrum disorders (ASDs), encodes 
a brain-specific T-box transcription factor. It is therefore possible that TBR1 
controls the expression of other autism risk factors. The downstream genes of 
TBR1 have been identified using microarray and promoter analyses. In this study, 
we annotated individual genes downstream of TBR1 and investigated any 
associations with ASDs through extensive literature searches. Of 124 TBR1 target 
genes, 23 were reported to be associated with ASDs. In addition, one gene, 
Kiaa0319, is a known causative gene for dyslexia, a disorder frequently 
associated with autism. A change in expression level in 10 of these 24 genes has 
been previously confirmed. We further validated the alteration of RNA expression 
levels of Kiaa0319, Baiap2, and Gad1 in Tbr1 deficient mice. Among these 24 
genes, four transcription factors Auts2, Nfia, Nr4a2, and Sox5 were found, 
suggesting that TBR1 controls a transcriptional cascade relevant to autism 
pathogenesis. A further five of the 24 genes (Cd44, Cdh8, Cntn6, Gpc6, and 
Ntng1) encode membrane proteins that regulate cell adhesion and axonal 
outgrowth. These genes likely contribute to the role of TBR1 in regulation of 
neuronal migration and axonal extension. Besides, decreases in Grin2b expression 
and increases in Gad1 expression imply that neuronal activity may be aberrant in 
Tbr1 deficient mice. These analyses provide direction for future experiments to 
reveal the pathogenic mechanism of autism.