Fig. S3

Cheng et al., 2016 - Vinculin b deficiency causes epicardial hyperplasia and coronary vessel disorganization in zebrafish
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Fig. S3

Vclbdel17 mutant exhibits the same phenotype as v12 mutant. (A) In vclbdel17 mutants, a17-bp deletion in vclb gene was created using CRISPR/Cas9 technology. The deletion removes a BglII site in vclb gene used for genotyping. (B) At 3dpf, vclbdel17 mutant shows similar pericardiac edema and pleural effusion in v12 mutant. (C) At 30 dpf, vclbdel17 mutant has craniofacial defects resembling v12 mutant. (D-G) vclbdel17 mutant shows increased epicardial expansion and Aldh1a2 expression at 40 dpf (E)and up-regulation of pERKin the endocardium at 55 dpf(G), both are similar to v12 mutant. Wildtype sibling controls are shown at the same stages (D, F). MF20 labels cardiomyocytes and DAPI labels nuclei. (H-M) vclbdel17 mutant shares similar coronary vessel defects with v12 mutant as indicated with a Tg(fli1a:EGFP) transgenic reporter, which labels endothelial cells. (N-N',O-O') Tg(tcf21:dsRed) transgenic reporter, which labels epicardial cells. vclbdel17 mutant shows similar over-proliferation of epicardial derived cells in v12 mutant. Scale bar:20μm(D-G, L-O'), 100μm(H-K).

Expression Data

Expression Detail
Antibody Labeling
Phenotype Data

Phenotype Detail
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