Figure 1. aplnra mutant embryos display defects in endoderm and heart formation.

(A) Schematic detailing the aplnra^max and aplnra^ins alleles. TM indicates the transmembrane domain. (B–E) Gross morphology of aplnra^max,aplnra^ins and aplnra^ins; aplnrb^hu4145 mutant embryos compared to WT (wild type) at 48 hpf (hours post-fertilization). (F–I) nkx2.5 expression at the 15 somite stage in WT, aplnrb^hu4145, aplnra^ins, and aplnra^ins; aplnrb^hu4145 mutant embryos. Dorsal view with anterior to the top. (J–L) In situ hybridization showing expression of myl7 at 48 hpf in aplnra^ins and aplnra^ins; aplnrb^hu4145 embryos compared to WT when viewed from the anterior. (M–P) Comparison of sox17 expression at 8 hpf between WT, aplnra^ins, aplnrb^hu4145and aplnra^ins; aplnrb^hu4145 mutant embryos. Dorsal views are shown with a lateral view in inset panels.

DOI: http://dx.doi.org/10.7554/eLife.13758.003

Figure 1—figure supplement 1. aplnra and aplnra; aplnrb double mutant characterization.

(A–D) Wholemount RNA in situ hybridization (WISH) showing expression of sox17 at 8 hpf and myl7 at 24 hpf in aplnra^max embryos compared to WT. (E–F) Quantification of the number and spread of sox17-positive cells in WT, aplnra^ins, aplnrb^hu4145and aplnra^ins; aplnrb^hu4145 embryos at 8 hpf. Data are represented as means ± SEM. *p<0.05, **p<0.01, n.s. = not significant unpaired two-tailed t-test.

DOI: http://dx.doi.org/10.7554/eLife.13758.004

Figure 1—figure supplement 2. aplnra; aplnrb double mutants display defects in endodermal organ development.

(A–I) WISH showing expression of foxa1 (A–C), foxa2 (D–F) and foxa3 (G–I) at 48 hpf in WT and aplnra^ins; aplnrb^hu4145 homozygous mutant embryos. P indicates the pancreatic bud, L indicates the liver bud and the arrow indicates the most anterior pharyngeal endoderm. For double mutants, two representative images are shown for each probe (n=7 for each marker). Embryos are visualized ventrally.

DOI: http://dx.doi.org/10.7554/eLife.13758.005