Fig. 2

Fig. 2 The liver defects in VPA-treated embryos correlated with inhibition in HDAC enzymatic activity. (a) HDAC enzymatic activity in zebrafish embryos were measured by fluorescent based assay. Embryos were treated (from 15-somite stage) with VPA (20 μM) and harvested at different stages. Total HDAC enzymatic activity was inhibited from 1 dpf onward and maximum reduction (around 75%) was observed at 2–3 dpf in VPA-treated embryos. (b) Embryos from Tg(lfabp:RFP; elaA:EGFP) were treated with TSA (B, D, G), a structurally unrelated HDAC inhibitor, and Valpromide (VPM) (C, E, H), a structural analogue of VPA which does not inhibit HDAC. Liver formation was observed at 3 dpf (A–C), 4 dpf (D–E) and 5 dpf (F–H). No liver was observed in TSA-treated embryos up to 4 dpf (B, D) while a small liver appeared at 5dpf (G, white arrow). Liver formation was unaffected in VPM-treated embryos (C–H, white arrows). All the images are lateral view, anterior to the left. Scale bar is 50 μm.