Figure 2

Zebrafish embryos displayed telencephalic malformations after knockdown of Pcgf1. (A) Western blot analysis of the specificity and efficiency of Pcgf1 knockdown in zebrafish at 24 hpf. The Pcgf1 MO could efficiently knockdown the expression of Pcgf1 because the expression of GFP is downregulated. The bar graphs clarified the relative level of GFP/actin expression for at least three independent experiments. Values represent mean ± SEM. ^**P < 0.01. (B) Compared with the embryos in the control group, the development of neural tube in the experimental group (MO) had obvious defects. The mild phenotype consisted of a smaller head and a shorter body axis, and the severe phenotype had a partial head area deletion. Bar graphs show the statistical data for the embryo numbers. ^**P < 0.01. (C) Morphology of Pcgf1 morphants at 16 and 24 hpf. The Pcgf1 MO group showed that the area of the telencephalon decreased or even disappeared compared with the control group. Co-injections of human Pcgf1 mRNA with Pcgf1 MO could partially rescue the telencephalic defects induced by Pcgf1 MO. Red line point to the telencephalic region. Scale bar: 200 μm.