Fig. 5

PI3K-Akt are crucial mediators for K-ras signaling in zebrafish hematopoiesis and angiogenesis.

(A) K-ras knockdown could be rescued by k-ras mRNA, but this rescue was suppressed by wortmannin at lower dose (250 nM). At this concentration, wortmannin itself could not induce hematopoietic defects in controlled phenol-red injected group. Embryo numbers n1 = 37, n2 = 38, n3 = 43 and n4 = 46, from two independent sets of experiments. (B) Hematopoietic defects caused by K-ras knockdown could be rescued by wild type K-ras and K-ras mutant k-rasC40 respectively. Embryo numbers n1 = 475, n2 = 344 and n3 = 80, from >4 independent sets of experiments. (C) Hematopoietic defects caused by K-ras knockdown could be rescued by Akt2 effectively. Embryo numbers n1 = 156 and n2 = 129, from 4 independent sets of experiment. * indicates p<0.05. (D) Angiogenic defects caused by K-ras knockdown could be rescued by wild type K-ras and K-ras mutant k-rasC40 respectively. Embryo numbers n1 = 133, n2 = 92 and n3 = 62, from >2 independent sets of experiments. (E) Angiogenic defects caused by K-ras knockdown could be rescued by Akt2. Embryo numbers n1 = 36, n2 = 20, each group from 2 independent sets of experiments. ** indicates p<0.10. All data are means±SD (standard deviation). Values indicated by the same letter are not significantly different at p<0.01 for (A) and (B), and at p<0.05 for (D).