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. Author manuscript; available in PMC: 2016 Jun 6.
Published in final edited form as: Am J Med Genet B Neuropsychiatr Genet. 2006 Jan;141(1):67–70. doi: 10.1002/ajmg.b.30229

Fig. 1.

Fig. 1

Expression analysis of PCDH11X/Y in the human brain. Specific RT-PCRs were performed on total RNA from different brain regions using primers with identical sequences for both PCDH11X and PCDH11Y. Discrimination between PCDH11X and PCDH11Y mRNA was done by restriction analysis taking advantage of a BsaAI site present only in the PCDH11X sequence. Primers in exons 4 and 5 (top panel) amplified the E4E5 transcript, which contains the two exons (E4 and E5) retained in all isoforms of both PCDH11X and PCDH11Y. Primers in exons 3 and 5 (middle panel) amplified the isoforms retaining exon 3 and originating from the promoter upstream of exon 1. Primers in exons 4.1 and 5 (bottom panel) amplified the isoforms originating from the promoter upstream of exon 4.1 and specific to the PCDH11Y gene. Normal control human brains were obtained at autopsy under guidelines approved by the Ethics Committee. The ages of the two males and the two females studied were 74, 42, 55, and 36 year-old, with a post-mortem delay of 10, 21, 24, and 2 hr, respectively. f: frontal cortex, tc: temporal cortex, o: occipital cortex, h: hippocampus, t: thalamus; c: cerebellum.