Figure 2: PP1 inhibition up-regulates pre-miR-183/96/182 expression. | Nature Communications

Figure 2: PP1 inhibition up-regulates pre-miR-183/96/182 expression.

From: The microRNA cluster miR-183/96/182 contributes to long-term memory in a protein phosphatase 1-dependent manner

Figure 2

(a) Pre-miR-183/96/182 expression in the nuclear fraction of the hippocampus from NIPP1* and control mice (pre-miR-183: controls, n=11; NIPP1*, n=11; t20=2.12, *P<0.05; pre-miR-182: controls, n=11; NIPP1*, n=11; t20=2.92, **P<0.01). (b) Cytoplasmic pre-miR-183/96/182 level in the hippocampus of NIPP1* mice and control littermates (pre-miR-183: t10=2.05, #P<0.1; pre-miR-182: t10=2.09, #P<0.1; controls, n=6; NIPP1, n=6). (c) PP1γ knockdown combined with KCl stimulation (1 h) causes upregulation of pre-miR-183, pre-miR-96, and pre-miR-182, which is reversed by PP1γ overexpression (pre-miR-183: one-way ANOVA, F2,6=3.12, P=0.12; t-test: t(4)=3.09, *P<0.05; pre-miR-96: one-way ANOVA, F2,6=9.19, P=0.01; t-test: t(4)=3.75, *P<0.05; pre-miR-182: one-way ANOVA, F2,6=4.13, P=0.07; t-test: t(4)=3.52, *P<0.05). (d) Nuclear pri-miRNA regulation by PP1γ knockdown and the effect of ActD treatment in N2A cells after 1 h of KCl stimulation (two-way ANOVA, ActD: F1,8=35.62, ***P<0.001, PP1γ: F1,8=5.37, P<0.05, post-hoc: vehicle **P≤0.01). (e) ActD treatment of N2A cells does not fully abolish pre-miRNA upregulation induced by PP1γ knockdown; left panel: pre-miR-183, two-way ANOVA: PP1γ-F(1,27)=17.6, P=0.0003 (post-hoc: vehicle t27=3.13, **P<0.01; ActD t27=2.85, **P<0.01); middle panel: pre-miR-96, two-way ANOVA: PP1γ-F(1,27)=16.1, P<0.001 (post-hoc, vehicle t27=4.05, ***P<0.001; ActD t27=1.8, #P<0.1); right panel: pre-miR-182, two-way ANOVA: PP1γ-F(1,28)=21.3, P<0.0001 (post-hoc, vehicle t28=3.45, **P<0.01;ActD t28=3.11, **P<0.01). Bar graphs represent mean±s.e.m.

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