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. 2021 May 11;12:2705. doi: 10.1038/s41467-021-23055-6

Fig. 7. ADP-ribosylation and macrodomain function contribute to AR-dependent transcription.

Fig. 7

a qPCR of AR target genes in control (shGFP) and Parp7-depleted (shParp7) VCaP cells, untreated (blue) and androgen-treated (red). The data were analyzed by an unpaired, two-tailed t test and are plotted as the mean + s.d. Dots represent individual values. For each treatment group, n = 3 biologically independent samples. b Scheme for testing the effects of Parp9 MD and AR ADP-ribosylation mutants on androgen-induced transcription from the PSA promoter. c Parp9 MD function is required for AR-dependent transcription. Parp9 knockout cells (PC3-AR background) were reconstituted with WT and mutant (G112, 311E) forms of Parp9, and AR activity measured using the 6-kB PSA promoter fused to firefly luciferase. Data were normalized to CMV-Renilla luciferase and Parp9 levels examined by immunoblotting. Color scheme is the same as a. The data were analyzed by an unpaired, two-tailed t test and are plotted as the mean + s.d. Dots represent individual values. For each treatment group, n = 3 biologically independent samples. d Mutation of ADP-ribosylation sites reduces AR-dependent transcription. AR-negative PC3M-HA-Parp7 cells were reconstituted with WT and mutant (4CG, 7CG, 8CG) forms of AR, and analyzed as described in c. The data were analyzed by an unpaired, two-tailed t test and are plotted as the mean + s.d. The color scheme is the same as a. Dots represent individual values. For each treatment group, n = 3 biologically independent samples. Source data are provided as a Source data file.