Effects of F5 deficiency on hemostasis in the venous and arterial circulation. (A) Laser-mediated endothelial injury of the PCV was performed on larvae at 3 dpf. The time to occlusion was significantly prolonged in f5^−/− larvae in comparison with f5^+/− and f5^+/+ siblings (P < .0001, Mann-Whitney U test). (B-C) Endothelial injury was also performed on the dorsal aorta at 9 dpf, and PMBC at 6 to 7 dpf with similar results. (D) Injection of wild-type zebrafish f5 cDNA under control of the zebrafish ubiquitin promoter into 1-cell stage embryos resulted in significant rescue of the PCV hemostatic defect at 3 dpf in 73% of f5^−/− larvae when compared with uninjected mutants (P < .001). Note that variability in the time to occlusion is a result of technical factors and heterozygosity in the genetic background. This has been seen with laser injury across other zebrafish mutants.