Fig. 6

arpl18 sibling and mutant embryos were treated with BP (T3708, STAT3 inhibitor) or AZ (T6309, JAK2 inhibitor) (N = 5). At 3 dpf, o-dianisidine staining of mutant embryos showed obvious recovery with BP (2.5 μM) treatment, and mutants treated with AZ (0.1 μM) also be seen partially restored (arrowhead). b The total amounts of Stat3 (t-Stat3) and the phosphorylation status of endogenous Stat3 protein (p-Stat3) was evaluated in rpl18 siblings and mutants. The protein levels of t-Stat3 and p-Stat3 had a significant increase in mutants, compared with wild-type (WT) embryos at 30 hpf. Both the t-Stat3 and p-Stat3 were dramatically decreased in Rpl18-deficient embryos treated with BP or AZ separately, as shown by western blotting. c The scatter diagram represented quantification of western blots. The results of three groups of experiments (twice technical repeated for each group) were statistically analyzed, *P < 0.05. d The o-dianisidine staining displayed that most of erythroid cells disappeared (arrow) in wild-type embryos after injection the STAT3CA (constitutively active STAT3 with the double mutation A661C N663C) mRNA, compared with sibling embryos at 3 dpf (N = 3). e Erythrocytes were partially rescued in rpl18 mutants that had been injected with STAT3DN (dominant-negative STAT3) mRNA at 3 dpf (N = 3). Black arrowhead points to the recovery of erythrocytes. f Model of the defective erythroid maturation in Rpl18 deficiency through increased phosphorylated Stat3 expression. All scale bars represent 250 μm.