Fig. 1.

Heart defect in a tadpole after sustained spib morpholino inhibition of myeloid cell differentiation. (A–E) X. laevisTg[lurp1:egfp] tadpole that was injected with Xtspib-e1i1MO into dorsal blastomeres, 40 ng dose. Tadpole was photographed at stage 40 (A and B) and stage 41 (C–E), with fluorescence from eGFP shown (B and D). The complete inhibition of myeloid cell differentiation caused by loss of spib has been sustained to stage 40. A large edema formed during this time interval, indicative of cardiac dysfunction (A, C, E). (F–J) Control sibling tadpole that was injected with the same morpholino into ventral blastomeres, photographed at stage 40 (F and G) and stage 41 (H–J). Fluorescent embryonic macrophages can be seen distributed throughout the tadpole (G and I). Hematopoiesis also observed in pronephros and liver (G and I). No edema developed and heart morphology appeared normal. Anterior is to the left in lateral (A–D, F–I) and ventral (E and J) views. Ed, edema; M, myeloid/macrophage; PN, pronephros; Lv, liver; MB and HB, additional domains of Tg[lurp1:egfp] fluorescence in mid and hindbrain.