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. Author manuscript; available in PMC: 2017 Apr 1.
Published in final edited form as: Genes Brain Behav. 2016 Apr;15(4):367–381. doi: 10.1111/gbb.12289

Figure 7. Confirmation of differential regulation of Ninein in the NAc.

Figure 7

a) Basal mRNA levels of Nin were significantly greater in D2 mice than B6 mice (*p<0.01, n=8 per group, Student’s t-test between strain) as confirmed by qRT-PCR. Nin expression was normalized to Ppp2r2a. b) Pyrosequencing of NAc samples of B6D2F1/J hybrid mice for an amplicon of Nin containing two progenitor SNPs confirmed cis regulation of Nin (*p<0.01, n=2 pooled per sample, n= 3 per group, n >4000 reads per group, Student’s t-test). c-d) Immunoblotting of NAc samples from untreated B6 and D2 mice revealed significantly higher levels of two isoforms (NIN4 and NIN5, ~120 KDa) in D2 mice compared to B6 (*p<0.05, Student’s t-test, n=5/strain). D2 mice also show a trend for higher levels of NIN6, NIN8, and NIN10 isoforms (p=0.1703, p=0.0589, p=0.1516, respectively, Student’s t-test). NIN levels were normalized to ACTB protein levels.