Fig. 6: Late DNA methylation inhibition activates p53 and in turn reduces BPPC redifferentiation through Bmp signaling.
From: DNA methylation maintenance at the p53 locus initiates biliary-mediated liver regeneration
a WISH images showing the expressions of id2a, tbx2b, and smad5 at R24h treated with DMSO or 5azaC in p53 mutant and wild-type livers (arrows). Quantification of the intensity of id2a, tbx2b, and smad5 expressions in liver regions at R24h. Note that the expressions of id2a, tbx2b, and smad5 were recovered in p53 mutant compared with control after 5azaC treatment. b Experimental scheme illustrating the 5azaC and Mtz treatment in transgenic line Tg(lfabp:Dendra2-NTR; hsp70l:Bmp2b) and heat shock from R8h to R48h. c Confocal images showing the regenerating livers at R48h after heat-shock and 5azaC treatment. d WISH images showing the expressions of gc and cp at R48h after heat-shock and 5azaC treatment. Quantification of the intensity of gc and cp expressions in liver regions at R48h. e Single-optical section images showing the expressions of hepatocyte marker Bhmt and BECs marker Alcam at R48h after heat-shock and 5azaC treatment. Quantification of the intensity of Bhmt expression and the percentage of Alcam+ among Dendra2+ cells in liver regions at R48h. Asterisks indicate statistical significance: **P < 0.01; ***P < 0.001; ****P < 0.0001 using t-tests analysis when compared to control. Numbers indicate the proportion of larvae exhibiting the expression shown. Scale bars: 100 µm; error bars, ±SEM. DAPI 4′,6-diamidino-2-phenylindole, BT before treatment, HS heat shock, OE overexpression, R regeneration time after the withdrawal of Mtz.
