Fig. 4: PGC-1α gene promoter activation by GSK3β and associated factors.
From: Neuron-specific isoform of PGC-1α regulates neuronal metabolism and brain aging
A RT-qPCR detection of PGC-1α transcripts in control and LiCl-treated neurons (n = 6 replicates). B RT-qPCR detection of PGC-1α transcripts after 24-h treatment with actinomycin D +/− LiCl (n = 7 replicates). C Immunoblots of phosphorylation and total protein of GSK3β, CREB, and AMPK after 24-h treatment with 15 mM lithium chloride (LiCl) (n = 6–7). D Prediction of CREB binding sequences in Mmu Ppargc1a promoters using a transcription factor binding motif prediction software (http://tfbind.hgc.jp/). E Schematic of proposed pathways of lithium regulation of Ppargc1a transcripts (orange—proteins investigated in (F–I). F–I RT-qPCR detection of Pparc-1a transcripts following treatment with lithium in the presence or absence of GSK3β inhibitor VIII (n = 6–8) (F), AMPK inhibitor Compound C (n = 5–9) (G), TrkB inhibitor ANA-12 (n = 4–6) (H), or CREB inhibitor 666-15 (I) (n = 6) (see Source data file for specific p-values for (F–I). J Heatmap of the significantly changing genes detected from the “Transcriptional corepressor binding” and “Transcriptional repressor complex” GO terms. Data shown with error bars noting mean ± SEM (A, B, F–I). Asterisk (*) indicates p-value < 0.05 by two-way ANOVA with Sidak’s multiple comparison test (A), ordinary one-way ANOVA with Dunnett’s test (B, F–I), or two-tailed unpaired student’s t-test (C). See Source data file for exact p-values and for exact n for each group of (F–I). See methods for details on biological replicates used for RT-qPCR and western blots.
