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Fig. 1 | Molecular Autism

Fig. 1

From: Germline nuclear-predominant Pten murine model exhibits impaired social and perseverative behavior, microglial activation, and increased oxytocinergic activity

Fig. 1

Characterization of gross morphological and Pten localization phenotypes in PtenY68H/+ mice. a Visualization of single missense mutation in exon 3 of mouse Pten c.202 T > C, converting tyrosine (Y) residue 68 into histidine (H), which served to generate the germline PtenY68H/+ mouse model. b Nuclear-cytoplasmic fractionation performed on Pten+/+ and PtenY68H/+ mouse cortical tissue and visualized via Western blot, targeting Pten as well as Hsp90 (cytoplasmic), and Lamin A/C (nuclear) to demonstrate fraction purity. N = 4. c Quantification of nuclear-cytoplasmic Pten ratio from Western blot in panel b (Median∆N/CRatio = 0.20, 97% CI: 0.14–0.34, P = 0.029). d Immunofluorescence staining of mouse cortex, visualizing Pten (red), and DAPI (blue) in neurons of Pten+/+ and PtenY68H/+mice. e Quantification of panel d (Median = 0.22; 97% CI: 0.089–0.48; P = 0.079). f Representative gross anatomical image, showing brain volume and morphology of Pten+/+ and PtenY68H/+mice. g Quantification of total brain mass and body weight in grams (g) of Pten+/+and PtenY68H/+ (medianΔBrainMass = 0.15, 97% CI: 0.090–0.21, P < 0.0001). h Analysis of downstream Pten signaling in PtenY68H/+ cortex by Western blot. N = 8. i Quantification of Pten expression data from panel h (P < 0.0002). j Quantification of P-Akt levels from panel h (P < 0.0002). k Quantification of P-S6 expression data from panel h (P = 0.50). l Quantification of P-Erk1/2 expression data from panel h (P = 0.16)

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