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Fig. 6 Model of artery specification controlled by Rtk/Akt/Notch signaling. In this study, we created the first zebrafish model with loss-of-function mutations in all four Akt genes (aktΔ/Δ). We found that Akt signaling is required for specifying endothelial cell progenitors into arteries independently of other kinases. Notably, restoring Notch activity in the dorsal aorta compensates for Akt loss, suggesting that Akt acts upstream of Notch in artery specification during embryonic development. Pi3k, phosphatidylinositol 3-kinase; Rtk, receptor tyrosine kinase.
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