Hematopoietic defects in lpl mutants. a In situ hybridization with lpl antisense and sence probes in WT embryos at 2 dpf. b Diagram of lpl CRISPR target sites and the predicted truncated protein caused by the 2 nt deletion, which results in a codon shift and premature translation termination. c qPCR results of lpl and apoc2 mRNA expression in WT, apoc2 and lpl mutants at 5 dpf (n = 3 in each group). d Plasma TG levels in adult (9–15-month-old) male WT, apoc2 and lpl mutants (n = 5 in each group). e Peripheral blood cell count in adult (15-month-old) male WT, apoc2 and lpl mutants (n = 5 in each group). f Wright–Giemsa staining of blood smears from 6.3 dpf WT, apoc2 and lpl mutants. g, h Representative images and quantitative results of blood cell (yellow arrows) count in the caudal vein (outlined with white dashed lines) of WT, apoc2 and lpl mutants at 6.3 dpf (n = 5 in WT and apoc2 mut groups each; n = 6 in lpl mut group). i o-Dianisine staining of 52 hpf and 6.3 dpf WT, apoc2 and lpl mutant embryos. Scale bars, 200 μm in a; 20 μm in f, g, and 100 μm in i. Quantitative results are mean ± SEM; *P < 0.05 and ***P < 0.001 (Student’s t test)
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