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. 2019 Oct 10;13:458. doi: 10.3389/fncel.2019.00458

FIGURE 1.

FIGURE 1

Generation and characterization of Emx1-Cre;Shank3Δ14–16 mice. (A) PCR genotyping of Emx1-Cre;Shank3Δ14–16 mice. Note that the primer set targeting exons 13 and 14 generates a PCR band for the floxed allele (478 bp), and the primer set targeting general Cre generates a PCR band (272 bp) in Emx1-Cre;Shank3Δ14–16 mice, but not in WT mice. (B,C) Reduced levels of Shank3 protein variants in different brain regions of Emx1-Cre;Shank3Δ14–16 mice (12–13 weeks, male and female). Total brain lysates were analyzed by immunoblotting using a Shank3-specific antibody (#2036) (B). Neither the Shank3e isoform in the thalamus nor the Shank3c/d isoform in the striatum was quantified because of their low levels of expression in these regions. Th, thalamus; Str, striatum; Hpc, hippocampus; Ctx, cortex. cKO band signals normalized to α-tubulin are expressed relative to those from WT mice (C). Data are shown as mean ± SEM. n = 5 pairs (WT, cKO), ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, nd, not detectable, ns, not significant, and one sample t-test. (D,E) Normal levels of Shank1 and Shank2 protein variants in different brain regions of Emx1-Cre;Shank3Δ14– 16 mice (12–13 weeks, male and female). Total brain lysates were analyzed by immunoblotting using a Shank1-specific antibody (#2100) and Shank2-specific antibody (162 202, SYSY) (D). cKO band signals normalized to α-tubulin are expressed relative to those from WT mice (E). Data are shown as mean ± SEM. n = 5 pairs (WT, cKO), ns, not significant, and one sample t-test.