Fig. 7
Gene knockdowns investigate the roles of stat1a and stat1b in hematopoiesis. In situ hybridization with probes for scl (A-G), gata1 (H-N), spi1 (O-U), and mpo (V-Y) in 16 hpf embryos (A-C, H-J, O-Q) and 32 hpf embryos (D-F, K-M, R-T, V-X) injected with control sequence MO (A, D, H, K, O, R, V), stat1a MO (B, E, I, L, W), and stat1b MO (C, F, J, M, X). Quantitative PCR experiments (G, N, U, Y). Knockdown of stat1a did not alter the expression of the genes tested, but knockdown of stat1b led to increased expression of scl and gata1, markers of HSCs and erythrocytes, and to depressed expression of spi1 and mpo, markers of the myelocyte lineage. These results would be expected if normal stat1b activity helped promote a lineage switch from the erythroid to the myeloid lineage.
Reprinted from Mechanisms of Development, 128(7-10), Song, H., Yan, Y.L., Titus, T., He, X., and Postlethwait, J.H., The role of stat1b in zebrafish hematopoiesis, 442-56, Copyright (2011) with permission from Elsevier. Full text @ Mech. Dev.