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Fig. 2
Fer knockdown results in apparent vasculature blockage and accumulation of developing hematopoietic cells. At 30 somites, fer-MO1 embryos exhibit convergence extension defects along the anterior–posterior axis with red blood cells that are pooled in the posterior ICM region (A) with none present in the pumping heart (B), when compared to wildtypes ((C,D) respectively). By 48 hpf, the lack of circulating red blood cells and empty heart chambers is emphasized in the Fer knockdown embryos (E,F) compared to wildtype embryos (G,H). Agarose gel electrophoresis of fer-reverse transcription PCR from fer-MO1 injected embryos to demonstrate the blockage of Fer splicing at exon 9 (I).