Figure 5.
Figure 5. Absence of hemostasis in f10 mutant larvae. (A) Schematic diagram of laser-induced endothelial injury of the PCV at the 5th somite (s5) caudal to the anal pore in larvae at 3 dpf. Hemostasis was evaluated by documenting the time to occlusion ≤120 seconds (sec) after laser-induced endothelial injury. (B) The time to occlusion was significantly prolonged in f10−/− larvae in comparison with f10+/+and f10+/− siblings (P < .0001, Mann-Whitney U test). (C) Injection of wild-type zebrafish f10 complementary DNA (cDNA) under control of the ubi promoter into 1-cell–stage embryos resulted in significant rescue of the hemostatic defect in 72% of f10−/− larvae at 3 dpf when compared with uninjected mutants (P < .05). Horizontal bars represent the median time to occlusion. ns, not significant.

Absence of hemostasis in f10 mutant larvae. (A) Schematic diagram of laser-induced endothelial injury of the PCV at the 5th somite (s5) caudal to the anal pore in larvae at 3 dpf. Hemostasis was evaluated by documenting the time to occlusion ≤120 seconds (sec) after laser-induced endothelial injury. (B) The time to occlusion was significantly prolonged in f10−/− larvae in comparison with f10+/+and f10+/− siblings (P < .0001, Mann-Whitney U test). (C) Injection of wild-type zebrafish f10 complementary DNA (cDNA) under control of the ubi promoter into 1-cell–stage embryos resulted in significant rescue of the hemostatic defect in 72% of f10−/− larvae at 3 dpf when compared with uninjected mutants (P < .05). Horizontal bars represent the median time to occlusion. ns, not significant.

Close Modal

or Create an Account

Close Modal
Close Modal