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Fig. 2

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ZDB-IMAGE-080502-20
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Figures for Farooq et al., 2008
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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.

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Reprinted from Developmental Biology, 317(1), Farooq, M., Sulochana, K.N., Pan, X., To, J., Sheng, D., Gong, Z., and Ge, R., Histone deacetylase 3 (hdac3) is specifically required for liver development in zebrafish, 336-353, Copyright (2008) with permission from Elsevier. Full text @ Dev. Biol.