Mice were housed under standard condition and protocols approved by the University Committee on Use and Care of Animals (UCUCA). Mice carrying Snail1 alleles 17 (link) and mice with Snail1-LacZ knock-in alleles 23 (link) were generated and maintained in our laboratory. Tie2-Cre, Vav1-Cre, Dermo1-Cre and β-actin-GFP transgenic mice were obtained from Jackson Laboratory. VE-cadherin-Cre ERT2 transgenic mice were provided by ML Iruela-Arispe (University of California, Los Angeles) 66 (link). Littermate controls of both sexes were used in all experiments. All mouse strains were backcrossed into the C57BL/6J background for at least 7 generations. To inhibit Notch signaling in vivo, timed pregnant mice were injected subcutaneously with 100 mg/kg DAPT (Tocris Bioscience) dissolved in 10% ethanol and 90% corn oil at E7.5, E8.5 and E9.5 with the embryos dissected at E10.5 6 (link). Gene inactivation in Snail1LacZ/fl;VE-cadherin-Cre-ERT2+ embryos was triggered by i.p. injections of 150 μl of tamoxifen solution (10 mg/ml, dissolved in 1:10 ethanol/corn oil; Sigma) into pregnant females at E11.5 and E13.5. Gene inactivation in pups was triggered by i.p. injections of 50 μl tamoxifen solution (10 mg/ml) at p1 and p3. Eyes were retrieved from pups at p6 and fixed in 4% paraformaldehyde-PBS overnight at 4°C. Retinas were dissected and subjected to whole-mount PECAM-1.