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. 2021 Sep 21;12(9):1460. doi: 10.3390/genes12091460

Figure 2.

Figure 2

ACLY-dependent up-regulation of Acetyl-CoA responsive genes in SIRT6 deficient U2OS cells. (A). Expression of acetyl-CoA responsive genes in control and SIRT6 KO cells normalized to GAPDH (Mean ± SEM of four independent experiments, ** p < 0.01, two-tailed Student’s t-test). (B). Increased PDGFRA protein levels in SIRT6 deficient cells compared to control cells. (C). Expression of glycolytic genes in control and SIRT6 KO cells normalized to GAPDH (Mean ± SEM of three independent experiments, ** p < 0.01, two-tailed Student’s t-test). (D). Increased expression of PDGFRA but not LDHA in SIRT6 KO cells is attenuated by ACLY inhibitor (ACLYi, 50 uM; 24 h). Data are normalized to GAPDH and show Mean ± SEM of four independent experiments, * p < 0.05, ** p < 0.01, ns: not significant, two-tailed Student’s t-test. (E). Increased H3 acetylation marks on PDGFRA promoter regions by ChIP-qPCR, attenuated by ACLY inhibitor (Mean ± SEM of three independent experiments, * p < 0.05, ** p < 0.01, ns: not significant, two-tailed Student’s t-test). (F). Increased H3 acetylation marks on LDHA gene promoter regions by ChIP-qPCR, independent of ACLY inhibition (Mean ± SEM of three independent experiments, ** p < 0.01, ns: not significant, two-tailed Student’s t-test).