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Mice lacking the 4 th -group paralog  Hoxd4  display malformations of the anterior vertebral column, but are viable and fertile. Here, we report that zebrafish embryos having decreased function of the orthologous  hoxd4a  gene manifest striking perturbations in vasculogenesis, angiogenesis and primitive and definitive hematopoiesis. These defects are preceded by reduced expression of the hemangioblast markers  scl1 ,  lmo2  and  fli1  within the posterior lateral plate mesoderm (PLM) at 13 hours post fertilization (hpf). Epistasis analysis revealed that  hoxd4a  acts upstream of  meis1.1  but downstream of  cdx4  as early as the shield stage in ventral-most mesoderm fated to give rise to hemangioblasts, leading us to propose that loss of  hoxd4a  function disrupts hemangioblast specification. These findings place  hoxd4a  high in a genetic hierarchy directing hemangioblast formation downstream of  cdx1 / cdx4  and upstream of  meis1.1 . An additional consequence of impaired  hoxd4a  and  meis1.1  expression is the deregulation of multiple Hox genes implicated in vasculogenesis and hematopoiesis which may further contribute to the defects described here. Our results add to evidence implicating key roles for Hox genes in their initial phase of expression early in gastrulation.

Zebrafish hoxd4a Acts Upstream of meis1.1 to Direct Vasculogenesis, Angiogenesis and Hematopoiesis