Fig. 3: Functional β-catenin responsive element in the Nlgn3 promoter. | Translational Psychiatry

Fig. 3: Functional β-catenin responsive element in the Nlgn3 promoter.

From: Wnt/β-catenin signaling stimulates the expression and synaptic clustering of the autism-associated Neuroligin 3 gene

Fig. 3

a Top panel: Representation of the 1.4 kb mouse Nlng3 promoter construct depicting the five TBE sites analyzed by ChIP assays. Bottom panel: Endogenous β-catenin binding to TBE Sites in the mouse Nlgn3 promoter examined in HT22 cells after treatment with either Wnt3a-CM for 4 h (left) or 20 mM LiCl for 24 h (right). Data represent mean ± s.e.m., **P < 0.01, ***P < 0.001, two-tailed Mann–Whitney test. b TBE sites (II–VI) were similarly examined by ChIP assays in HT22 cells under control conditions or treated with 1 µM CHIR 98014 for 4 h. In (a and b) immunoglobulin G (IgG) was used as a control. c Top panel: Representation of changes introduced by site-directed mutagenesis in TBE Sites II and III in the context of the 1.4 kb mouse Nlng3 promoter construct. TBE consensus sequence: CTTTG; Mutated TBE sequence: CCTCG. Bottom panel: Transient transfection of increasing doses of mutant plasmids in the presence of constitutively active β-catenin (S33Y) in HEK293 cells for 24 h. RLU: relative luciferase units. Data represent mean ± s.e.m., *P < 0.05, one-way ANOVA and Kruskal–Wallis post hoc test. ns not significant

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