(A) Experiment schematic: 32-cell stage injected to target either HPCs (red) or the anterior endoderm (yellow). (B–D) Transgenic nkx2.5-GFP embryos co-injected with endoderm-targeted arhgef-C55R mRNA and rhodamine dextran (RDA) (B) (scale bar, 1 mm). Cardiac differentiation proceeds but arhgef2-C55R reduces AP length (C) and increases rates of pericardial edemas per clutch (D) (n = 23 control, 35 arhgef2-C55R, over three clutches). (E) Compliance of arhgef-C55R is reduced (n = 8–9 embryos over two clutches). (F) Upper: tropomyosin, aPKC, and RDA. Lower: tropomyosin-masked aPKC expression in pseudocolor LUT (scale bar, 50 μm). Apical aPKC is increased in arhgef2-C55R, whereas Y27632 treatment can reverse the effect (n = 7–11 embryos over three clutches). (G) Representative confocal sections of stage 39 tadpole heart morphology (scale bar, 100 μm). Note: errant RDA/arhgef-C55R cell (asterisk) in coelom outside heart. Error bars represent mean ± SEM. ∗p < 0.05, ∗∗p < 0.01. See also Figures S1, S3B, S4, and S5.
Image published in: Jackson TR et al. (2017)
Copyright © 2017. Image reproduced with permission of the Publisher, Elsevier B. V.
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