Fig. 2

ccbe1, vegfc and vegfr3 genetically interact in double and triple heterozygous animals. (A-H) Confocal projections of Tg(fli1a:EGFP; kdr-l:mCherry) show grossly unaltered overall morphology and blood vasculature in ccbe1^hu3613 (B), vegfr3^hu4602 (E) and vegfc^hu5055 (F) mutants compared with wild type (A). The TD (C, arrows) is absent in ccbe1^hu3613 (D), vegfr3 ^hu4602 (G) and vegfc ^hu5055 (H) mutants (asterisks). (I-K) ccbe1, vegfc and vegfr3 genetically interact in double heterozygote embryos, which display lymphatic defects. Offspring from vegfc^+/- and vegfr3^+/- carriers give rise to 28% of embryos (n=28/99) with a TD length of d50%. This population is significantly enriched (71%; n=20/28; P<0.0001) in double heterozygotes (I). Similarly in ccbe1^+/- and vegfr3^+/- crosses, 24% (n=24/100) embryos develop d50% of their TD, and again this population is significantly enriched (54%; n=13/24; P=0.0098) in double heterozygotes (J). In ccbe1^+/- and vegfc^+/- crosses, 14% (n=18/126) of embryos develop d50% of their TD, this population being significantly enriched (61%; n=11/18; P=0.0096) in double heterozygotes (K). (L) Crossing double heterozygous ccbe1^+/-; vegfr3^+/- animals to vegfc^+/- animals, results in 21% (n=25/121) of embryos with d50% of TD: within this population, 40% (n=10/25; P=0.0004) of the embryos were triple heterozygotes, a significant enrichment from the statistical triple heterozygosity rate of 15%.