Fig. 7: Binding site mutations on TEN2 selectively abolish excitatory but not inhibitory synapse formation. | Nature Communications

Fig. 7: Binding site mutations on TEN2 selectively abolish excitatory but not inhibitory synapse formation.

From: Alternative splicing controls teneurin-latrophilin interaction and synapse specificity by a shape-shifting mechanism

Fig. 7

a Diagram for TEN2 DHR −SS and TEN2 DHR +SS constructs that were used in the below experiments. The seven amino acid splice site on the TEN2 β-propeller is indicated by empty or filled red stars; DHR mutation is indicated by black dots. b, c Artificial synapse formation assay showing that LPHN-binding mutant (DHR) of TEN2 −SS attenuated excitatory synapse formation. HEK293T cells are co-transfected with indicated cell-adhesion molecules and GFP, and co-cultured with cortical neurons. Cultures were subsequently immunostained for the excitatory postsynaptic synapse marker PSD95. Representative images (b) and quantifications of PSD95 signals (c) are shown. d, e LPHN-binding mutant (DHR) of TEN2 +SS did not affect inhibitory synapse formation. Similar in b and c, except that immunostaining for the inhibitory postsynaptic synapse marker GABA(A)α2 was performed. Scale bar in b and d indicates 10 µm. Data in c and e are presented as mean ± SEM, n = 3, and are representative of at least three independent experiments. ns, P > 0.05; *P < 0.05 (one-way ANOVA). Source data are provided as a Source Data file.

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