Fig. 1
- ID
- ZDB-FIG-180912-63
- Publication
- Berenguer et al., 2018 - Mouse but not zebrafish requires retinoic acid for control of neuromesodermal progenitors and body axis extension
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Loss of RA synthesis does not perturb zebrafish body axis extension. (A) Embryos treated with DMSO (control), 4 μM DEAB, or 10 μM DEAB from 5 to 15 hpf, followed by analysis of myoD expression. Brackets mark an 8 somite region in each embryo that is unchanged in length along the anteroposterior axis following DEAB treatment used to inhibit RA synthesis. (B) Embryos treated as described above from 5 to 15 hpf followed by a return to normal growth medium until 32 hpf. Arrows point to the heart region showing cardiac edema in embryos treated with DEAB. (C) Shown are embryos treated with DMSO (control) or 4 μM DEAB from 9.5 to 15 hpf followed by a return to normal growth medium until 72 hpf when it can be observed that DEAB treatment results in failure of pectoral fin outgrowth (arrows). (D) Comparison of body axis length along an 8-somite region in embryos at 15 hpf across the indicated treatment conditions; data are expressed as mean± SD. For all comparisons, p > 0.05 (not significant difference) using one-way ANOVA non-parametric test (DMSO control, n = 62; 4 μM DEAB n = 108; 10 μM DEAB n = 101; each are biological replicates). AU, arbitrary units. |
Reprinted from Developmental Biology, 441(1), Berenguer, M., Lancman, J.J., Cunningham, T.J., Duc Si Dong, P., Duester, G., Mouse but not zebrafish requires retinoic acid for control of neuromesodermal progenitors and body axis extension, 127-131, Copyright (2018) with permission from Elsevier. Full text @ Dev. Biol.