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. 2013 Feb 17;41(7):4129–4143. doi: 10.1093/nar/gkt093

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© The Author(s) 2013. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — Suppression of miR-23a blocks erythroid differentiation in zebrafish. (A) Manual alignment of mature miR-23a genomic sequences in five vertebrate species. Sequences derived from the miRBase database (Release 18). (B) qPCR analysis of miR-23a at 12, 24 and 48 h of zebrafish embryo development. Error bars represent standard deviation obtained from three independent experiments. (C) qPCR analysis of miR-23a in 10 somites and 24 hpf embryos after the indicated treatments. (*) Significant changes in embryos injected with the morpholino antagonist of miR-23a (miR-23a MO) compared with control morpholino (Ctrl MO) (*P < 0.05; **P < 0.01). (D) Lateral view of the heart and yolk sac of Ctrl MO- or miR-23a MO-injected embryos. (E) o-Dianisidine staining of hemoglobin in randomly selected 48 hpf embryos injected with Ctrl MO or miR-23a MO. (F) Expression of the hematopoietic lineage markers hbbe3 and scl in 10 somites embryos by whole-mount in situ hybridization. Randomly selected 10 somites embryos, injected with Ctrl MO or miR-23a MO, showing a normal degree of hbbe3 and scl staining in both groups. (G and H) Expression of gata-1 in 10 somites (G) and 24 hpf (H) embryos by whole-mount in situ hybridization. Randomly selected 10 somites and 24 hpf embryos, injected with Ctrl MO or miR-23a MO, showing a normal degree of gata-1 staining in both groups.