Inhibition of the erythroid transcriptional program enables expression of endothelial markers. All embryos were assayed by in situ hybridization at st32. Ventral views are presented for all embryos. MO treatment is indicated at the top of each column. (A-D) Knockdown of Gata2, Lmo2, or Tal1 activity reduced erythroid differentiation marker expression (hba1) relative to controls. (E-G) Specificity of MO knockdown was demonstrated by efficient rescue after coinjection of MO plus the cognate mRNA. (H-O) Knockdown of Gata2, Lmo2, or Tal1 resulted in high level expression of EC markers (aplnr and kdr) at the ventral midline compared with controls. Numbers at the lower right of each panel indicate the proportion of embryos displaying the illustrated phenotype.