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Fig. 1

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ZDB-IMAGE-100225-13
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Figures for Rai et al., 2010
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Fig. 1 Dnmt3 knockdown in zebrafish embryos results in neurogenesis defects. A, splice blocking by dnmt3 splice-blocking morpholino (dnmt3 Mo1) was monitored by RT-PCR in mRNAs from control and dnmt3 morphants at 80 hpf. PCR was performed using a forward primer in exon 6 and a reverse primer in exon 7. Note that the dnmt3 Mo1 stabilizes the unspliced transcript containing introns 6 and 7 (400 bp), whereas the spliced version (300 bp) is detected in control injected embryos. Percent knockdown (% KD) shown is the ratio of intensity of unspliced product to combined intensity of unspliced and spliced products normalized over β-actin intensity. B, morphology defects in dnmt3 morphants at 80 hpf. Note the smaller head, a pericardial edema, and a curled tail in dnmt3 morphants compared with control morphants. Bar equals 0.5 mm. C, whole mount in situ analysis of ngn-1, ascl1a, and ascl1b expression in dnmt3 morpholino alone or with p53 morpholino-, dnmt1 morpholino-, or control morpholino-injected embryos at 30 hpf. Whereas ngn-1 expression was normal in dnmt3 and dnmt1 morphants, ascl1a and ascl1b were selectively is absent. This defect can be complemented by co-injection of the wild-type (Dnmt3WT) but not by a catalytically inactive derivative (Dnmt3C1240S). D, protein expression levels of Dnmt3 wild-type (Dnmt3WT) and catalytically inactive (Dnmt3C1240S) derivatives. HEK293 cells were transfected with Dnmt3WT and Dnmt3C1240S, and Western blots were performed using antibodies against His tag. Both of these show equal expression of these derivatives. β-Actin was used as a loading control.

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Full text @ J. Biol. Chem.