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. Author manuscript; available in PMC: 2008 Jan 31.
Published in final edited form as: Mol Psychiatry. 2007 May 15;13(1):90–98. doi: 10.1038/sj.mp.4002016

Figure 3.

Figure 3

Association studies and transcript analyses of the ASMT gene. (a) Haplotype block structure of the ASMT gene. The relative physical position of each single nucleotide polymorphism (SNP) is given in the upper diagram, and the pairwise LD (D0) between all SNPs is given below each SNP combination. (b) Plot of the case–control P-values (−log10) for all variations studied within ASMT. 1: E1A; 2: rs4446909; 3: rs5989681; 4: P1BC; 5:rs6644635; 6: rs6588802; 7: rs28675287; 8: rs6588809; 9: I6A; 10: rs7471973; 11: rs5431942; 12: rs4933063; 13: rs11346829. SNPs located in promoter B are included in the shaded box. P-values for the risk haplotype GGGC are indicated as straight lines with close (cases vs controls) or open circles (transmission disequilibrium test (TDT)). (c) Quantification of ASMT transcripts relative to rs4446909 and rs5989681 genotypes (A represents the individuals with an A/A or A/G genotype; C represents the individuals with C/C or C/G genotype; G represents the individuals homozygous G/G). Black and white circles indicate individuals with autism spectrum disorders (ASD) and controls, respectively. The gray symbols indicate individuals homozygous A/A and C/C for rs4446909 and rs5989681, respectively. Real-time reverse transcriptase (RT)-PCR was performed with B lymphoblastoid cell lines from 38 ASD probands and 29 controls. Horizontal bars indicate medians. No statistical difference was observed between ASD and controls (Mann–Whitney U-test).