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. 2021 Jan 4;131(1):e139929. doi: 10.1172/JCI139929

Figure 8. GTP abundance regulates Pol I function in Mychi cells in part through GPN1 and GPN3.

Figure 8

(A) Nuclear RPA1 immunofluorescence signal in H82 cells with CRISPR/Cas9-mediated GPN3 knockout and reexpression of wild-type or mutant GPN3, treated with 1 μM MPA or vehicle for 12 hours. ***P < 0.001, NS, not significant. (B) Abundance of pre-rRNA in H82 cells with CRISPR/Cas9-mediated GPN3 knockout and reexpression of wild-type or mutant GPN3, treated with 0, 1, or 5 μM MPA for 8 hours. **P < 0.01, ***P < 0.001. (C) OP-Puro signal in H82 cells with CRISPR/Cas9-mediated GPN3 knockout and reexpression of wild-type or mutant GPN3, treated with 0, 1, or 5 μM MPA for 24 hours. A 30-minute cycloheximide treatment was used as a positive control. ***P < 0.001, ****P < 0.0001. (D and E) MPA IC50 in GPN3- or GPN1-deficient H82 cells reconstituted with empty vector (EV), wild-type, or mutant GPN3 or GPN1. **P < 0.01, ***P < 0.001. (F) GTP functions as a metabolic gate for Pol I function and ribosome biogenesis in cells with oncogenic MYC. Data are shown as mean and SD (A–E). Statistical significance was assessed using 1-way ANOVA with Tukey’s multiple-comparison test (A–E). All experiments were repeated twice or more.