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Fig. 3 | Acta Neuropathologica Communications

Fig. 3

From: Autism-linked mutations of CTTNBP2 reduce social interaction and impair dendritic spine formation via diverse mechanisms

Fig. 3

Interaction with cortactin via the C-terminal P-rich domain of CTTNBP2 is essential for dendritic spine formation and activity. a Cortactin overexpression rescues dendritic spine density in neurons expressing M120I or R533* mutant protein. HA-tagged WT, M120I or R533* CTTNBP2 was cotransfected with Myc-tagged cortactin (CTTN) and GFP-actin. In M120I- and R533*-transfected neurons, cortactin expression rescues dendritic spine density. Quantification results of dendritic spine density are shown. b Overexpression of the GFP-P-rich construct reduced the synaptic distribution of cortactin in mature cultured hippocampal neurons. The signal of cortactin in individual spines was normalized with the signal for cortactin in the soma to represent synaptic enrichment of cortactin. c Overexpression of the GFP-P-rich construct reduces dendritic spine density. d GFP-P-rich overexpression reduces mEPSC frequency, but not amplitude. GFP was used as a control in (b)–(d). Data represent mean ± SEM from three independent experiments. Each dot in (a, c), (b) and (d) represents an individual dendrite, spine or, neuron, respectively. Two-tailed unpaired t tests were performed. All statistical data and exact sample sizes are available in Additional file 2: Table S1. *P < 0.05; **P < 0.01; ***P < 0.001; ns, not significant. Scale bar: a upper, 20 μm; lower, 10 μm; b 5 μm; c upper, 20 μm; lower, 10 μm

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