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. 2016 Mar 22;25(11):2168–2181. doi: 10.1093/hmg/ddw084

Figure 5.

Figure 5.

Chondrolectin is a direct target of miR-431 and is decreased in SMN deficient motor neurons. ( A ) qRT-PCR of Chodl confirms reduced expression in SMN knockdown motor neurons. N = 8 from 4 experiments, *** P < 0.001, unpaired two-tailed Student’s t -test. ( B ) qRT-PCR in cortical neurons shows Chodl is not reduced. N = 7 from 3 experiments. ( C ) Schematic depiction of the evolutionary conservation of the miR-431 binding site (highlighted in red) in the Chodl 3′UTR in mammals. The site is predicted by both the TargetScan −0.29 and PITA −10.17 algorithms. ( D ) Transfection of anti-miR-431 in motor neurons increases Chodl expression. N = 6 from 3 experiments, ** P < 0.01, **** P < 0.0001, unpaired two-tailed Student’s t -test. ( E ) Transfection of a miR-431 mimic in motor neurons decreases expression of Chodl . N = 8 from 4 experiments. * P < 0.05, unpaired two-tailed Student’s t -test. ( F ) Schematic of control and mutated (highlighted in red) luciferase constructs of the binding site in the Chodl 3′UTR. ( G ) Relative Renilla /firefly luciferase expression following miR-431 mimic expression in Chodl3′UTR and Chodl3′UTRmut psicheck-2 transfected HEK293 cells at 24 h. Wild-type Chodl3′UTR N = 7 from 3 experiments. Chodl3′UTRmut N = 5 from two experiments. Significance was determined by two way ANOVA *** P < 0.001. Data are represented as mean ± SEM.