Loss of pros1 partially phenocopies the proc mutation. (A) Two sgRNAs were selected to target exons 1 and 11 (indicated by arrowheads) and resulted in an 8.3-kb deletion. (B) qPCR of pros1 expression demonstrated 45% and 93% reduction in heterozygous and homozygous mutants, respectively; n = 4 in each group. Data were analyzed by unpaired 2-tailed t test and plotted as mean ± standard error of the mean. (C) Mortality tracking showed no survival defect in pros1-null fish. Log-rank (Mantel-Cox) testing revealed no significant difference between each group. (D) Laser-mediated endothelial injury revealed a significant coagulation defect in pros1 mutants (P < .0001 by Mann-Whitney U testing). Bars indicate median TTO. (E) pros1 mutants demonstrate significant spontaneous venous thrombosis (Fishers exact test P = .001 between pros1^+/+ and pros1^−/−) but to a far lesser degree than proc mutants. (F) Representative light microscopic image reveals spontaneous thrombosis in the heart of a pros1^−/− mutant (scale bar, 100 μm), which was found in the majority of this group upon quantification (G). Fishers exact test P < .0001 between pros1^+/+ and pros1^−/−. All observations were performed by an observer blinded to genotype or condition. The fibrin deposition scale indicates the number of thrombi counted in each larva, binned into 4 groups.