Fig. 4: Tcf4 overexpression leads to an increase of premature spine numbers and proteome alterations in peripubertal mice.

a Experimental design. Group-housed Tcf4tg and wt mice were analyzed (*) at the age of 4 weeks (upper bar) (n = 4, each). Independent cohorts of Tcf4tg and wt mice were group-housed (middle bar) or exposed to chronic social defeat (SD, bottom bar) and analyzed at the age of 12 weeks (*). b Total spine density in the frontal cortex of Tcf4tg and wt mice was analyzed with STED nanoscopy. Spine density was significantly increased in 4-week-old Tcf4tg mice (p = 0.031). There was no difference in total spine density between the genotypes upon group housing (p = 0.686) or SD (p = 0.786) in 12-week-old mice. Subjecting mice to SD during puberty reduced total spine densities significantly (p = 0.003) without genotype differences. Data represent mean ± SEM. See Supplementary Fig. 6 for detailed analysis of spine types. c The analysis of electron-microscopic pictures for asymmetric/glutamatergic synapses reveals no differences between Tcf4tg and wt mice (n = 5, each). in the anterior cingulate cortex (ACC) nor the orbitofrontal cortex (OFC) at 4 weeks of age (p > 0.400). d Visualization of proteomic data from cytoplasmic and synaptosomal fractions isolated from frontal cortex of 4 weeks old Tcf4tg mice and wt controls (n = 4, each). Network graph of differentially regulated proteins in cytoplasmic (circular nodes), synaptosomal (diamond-shape nodes) and in both (hexagonal nodes) fractions. KEGG networks and overrepresented pathways visualized with ClueGo and CluePedia in Cytoscape are depicted as filled hexagons (blue = synapse associated pathways; grey = metabolic pathways). Primary data are from Supplementary Table 2.