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Fig. S2. PRDM12 acts as a transcriptional repressor (A) The structure of EnR-PRDM12 (top) and VP16-PRDM12 (bottom). Gray box, EnR domain; black box, VP16 domain; the silver-gray boxes, zinc finger domains. (B–E) Lateral view of each embryo at stage 38. Top right indicates the dorsal view of the head. (B) Control embryo. (C) Overexpression of VP16-PRDM12 mRNA (1000 pg/embryo) increased pigmentation (increased pigmentation in 57%, n=72). In contract, (D and E) the defect of pigmentation was observed in embryos injected with PRDM12-WT mRNA (1000 pg/embryo) and EnR-PRDM12 mRNA (1000 pg/embryo) (suppression in 55%, n=51, 58%, n=60, respectively). Scale bars represent 1 mm. (F and G) RT-PCR analysis of neural crest markers. (F) Embryos injected with PRDM12-WT mRNA (500 or 1000 pg/embryo) or VP16-PRDM12 mRNA (500 or 1000 pg/embryo) were harvested until stage 9 and dissected to obtain animal caps. The expression of neural crest markers was detected in VP16-PRDM12 mRNA-injected animal cap cells. (G) Embryos injected with Chordin (50 pg/embryo) and Wnt8 (50 pg/embryo) mRNAs with or without PRDM12-WT mRNA or EnR-PRDM12 mRNA were harvested until stage 9 and dissected. The effects of EnR-PRDM12 mRNA were similar to those of PRDM12-WT mRNA.

Image published in: Matsukawa S et al. (2015)

Copyright © 2015. Image reproduced with permission of the Publisher, Elsevier B. V.

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