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. 2014 May 27;124(7):2909–2920. doi: 10.1172/JCI74382

Figure 3. SLU7 is required for the preservation of the genetic program characteristic of the differentiated, quiescent, and metabolically functional liver.

Figure 3

(A) qPCR analysis of Slu7 expression in livers of mice infected with AAV-shSLU7 or control (AAV-Ren). ***P < 0.001. (B) Representative Western blot analysis of SLU7 protein in liver tissues. ACTIN levels are shown as control. Lanes were run on the same gel but were noncontiguous. (C) Effect of Slu7 knockdown in mouse liver on Srsf3 alternative splicing. Left: Representative gel analyzing Srsf3 Iso1 and Iso2 RT-PCR products. Right: qPCR analysis of Srsf3 Iso2/Iso1 ratio in livers. *P < 0.05 vs. AAV-Ren. (D) qPCR analysis of expression of selected liver-enriched genes along with the fetal and proliferative hepatocyte markers Afp, Wt1, and Atf3. *P < 0.05, **P < 0.01, ***P < 0.001 vs. AAV-Ren. (E) Liver-specific Slu7 knockdown induced a switch in the gene expression of metabolic enzymes, Hnf4α P1/P2 promoter usage, and Insr splicing isoforms toward a pattern characteristic of the fetal and transformed hepatocyte. *P < 0.05, **P < 0.01 vs. AAV-Ren. (F) Liver-specific Slu7 knockdown influenced serum levels of glucose, cholesterol, and triglycerides. *P < 0.05, **P < 0.01, ***P < 0.001 vs. AAV-Ren.