Fig. 1

Loss-of-function nol9 mutation leads to defects in the development of the intestine, liver, pancreas and definitive erythrocytes in zebrafish.

(A) Schematic representation of the nol9 gene and protein. Vertical bars represent exons (black boxes) and UTRs (grey boxes). The nonsense point mutation in nol9^sa1022 is marked in red. Wild-type Nol9 protein and its expected truncated version resulting from the nol9^sa1022 allele are shown. Domains of the Nol9 protein are indicated by grey boxes. P—P-loop NTP-ase domain. (B) Representative DIC images of nol9^+/+ and nol9^{sa1022/sa1022} larvae at 120 hpf. Left and right sides of each larva are shown. White arrow points to the liver. Black arrow shows the swim bladder. Pancreas is outlined in yellow. (C) Representative bright filed images of the intestinal folds at 120 hpf. The nol9^{sa1022/sa1022} mutant larvae have less developed intestinal folds (black arrowhead) compared to nol9^+/+ siblings. (D) Whole-mount in situ hybridization using hbae1 riboprobe at 120 hpf. Arrow indicates hbae1-positive definitive erythrocytes present in the CHT of nol9^+/sa1022 and nol9^+/+ but not nol9^{sa1022/sa1022} embryos. (E) Quantification of hbae1 in situ hybridization data. Data are represented as the number of larvae belonging to each phenotypic group. Fisher’s exact test, **, p<0.01.