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Loss of  Tbx4  results in absence of chorio-allantoic fusion and failure of formation of the primary vascular plexus of the allantois leading to embryonic death at E10.5. We reviewed the literature for genes implicated in chorio-allantoic fusion, cavitation and vascular plexus formation, processes affected in  Tbx4  mutant allantoises. Using this candidate gene approach, we identified a number of genes downstream of  Tbx4  in the allantois including extracellular matrix molecules  Vcan, Has2 , and  Itgα5 , transcription factors  Snai1  and  Twist , and signaling molecules  Bmp2 ,  Bmp7, Notch2, Jag1  and  Wnt2 . In addition, we show that the canonical Wnt signaling pathway contributes to the vessel-forming potential of the allantois.  Ex vivo , the  Tbx4  mutant phenotype can be rescued using agonists of the Wnt signaling pathway and, in wildtype allantoises, an inhibitor of the canonical Wnt signaling pathway disrupts vascular plexus formation.  In vivo ,  Tbx4  and  Wnt2  double heterozygous placentas show decreased vasculature suggesting interactions between  Tbx4  and the canonical Wnt signaling pathway in the process of allantois-derived blood vessel formation.

Candidate Gene Approach Identifies Multiple Genes and Signaling Pathways Downstream of Tbx4 in the Developing Allantois