Fig. 1

Fig. 1 Endocardial and cardiac valve defects were found in sco^te382 mutant embryos. (A,B) Brightfield views of live wild-type (A) and sco^te382 mutant (B) embryos at 48hpf. Note pericardial edema and heart abnormality (black arrowhead), as well as abnormal vessels in the caudal trunk (red arrowhead). (C,D) Confocal images of Tg(myl7:eGFP) transgenic wild-type (C) and sco^te382 mutant (D) hearts at 48hpf. Note lack of constricted AVC and dilated heart in sco^te382 mutant (arrowhead). (E,F) Hematoxylin-eosin staining of wild-type (E) and sco^te382 mutant (F) hearts at 48hpf on transverse JB4 sections. Note lack of AVC constriction (arrowhead) in sco^te382 mutant heart. (G,H) Valve leaflets (arrowhead) were labeled and detected by the Tg(kdrl:eGFP) transgene in wild-type (G), but not in sco^te382 mutant (H) embryos at 6dpf on vibrotome sections across the heart. (I–N) Endocardial markers fli1 (I,J) and tie1 (K,L) were expressed in wild-type (I,K) and sco^te382 mutant (J,L) embryos; and Tg(kdrl:eGFP) labeled the endocardium in wild type (M) and sco^te382 mutant (N) embryos at 48hpf. Note that endocardial genes (fli1, tie1 and flk1) were reduced in the atrium of sco^te382 mutants (J,L,N). Arrows point to the AVC. a, atrium; v, ventricle.