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. 2013 Apr 18;9(4):e1003461. doi: 10.1371/journal.pgen.1003461

Figure 7. Loss of Jarid1b leads to increased global levels of H3K4me3 and higher expression of key developmental regulators during embryogenesis.

Figure 7

(A) Immunoblots for Jarid1b and H3K4me3 of Jarid1b embryos at different developmental stages. Vinculin, H4 and Ponceau serve as loading controls. (B) Staining for β-galactosidase on sections of P0 brains representing Jarid1b expression. Staining of a wild-type brain is shown as negative control (boxed inset). Scale bar, 2 mm. (C) Expression of Jarid1b in fore- and hindbrains of wild-type, heterozygous and knockout newborns (normalized to β-actin). (D–G) Left: ChIP-qPCR for Jarid1b, H3K4me3, H3K27me3, H3 and IgG in forebrains of P0 pups. Error bars represent S.D. of three PCR amplifications. Right: Expression of indicated genes in forebrains analyzed by RT-qPCR (normalized to β-actin). Each dot represents an individual embryo. MaeI expression was below detection. One representative gene is shown for each chromatin state: (D) H3K27me3, (E) H3K4me3/H3K27me3, (F) H3K4me3 and (G) unmodified.