Figure 4.

Scrib1 mutation modulating ERK protein levels in the hippocampus and having a biphasic effect on the ERK signaling pathway. (A) Representative immunoblot illustration of CA1, CA3, and DG from control and social WT and Scrib^crc/+ mice analyzed simultaneously for phospho−ERK1/2 (pERK1/2) and ERK1/2. (B,C) Quantifications of phospho−ERK1 and phospho−ERK2 in CA1, CA3, and DG (2-way ANOVA; social WT vs. social Scrib^crc/+; pERK1/ERK1−CA3: F_1,12 = 6.41, * p < 0.05; social pERK2/ERK2−DG: F_1,16 = 8.96, ** p < 0.01; pERK2/ERK2−CA3: F_1,15 = 9.88, ** p < 0.01 for genotype x exposure interaction; n = 5–8 values per conditions). (D) Luciferase reporter assay data from HEK293 cells transfected with the SRE-LUC reporter vector, along with the increasing amount of the Scrib or Scrib^crc/+ expression plasmid as indicated (2−way ANOVA: F_11.132 = 217.4; *** p < 0.0001 for dose effect). Activation threshold of the serum-induced ERK pathway is indicated by the horizontal dashed line (Scrib vs. Scrib^crc, Bonferroni comparison t-test: 25 ng: t₁₆ = 13.68, *** p < 0.001; 50 ng: t₁₆ = 9.248, *** p < 0.001; 100 ng: t₃₄ = 8.57, *** p < 0.001; 250 ng: t₁₆ = 3.31, * p < 0.05; 500 ng: t₁₆ = 3.31, n.s; n = 9 values per condition). All data are presented as median with 25th and 75th percentiles, and single data points are shown as dots. The shaded area represents the probability distribution of the variable.