header logo image header logo text
Downloads Login
Research
General Information
ZIRC
ZFIN ID: ZDB-FIG-161110-12
Cheng et al., 2016 - Vinculin b deficiency causes epicardial hyperplasia and coronary vessel disorganization in zebrafish. Development (Cambridge, England)   143(19):3522-3531 Full text @ Development
ADDITIONAL FIGURES
EXPRESSION / LABELING:
Genes:
Antibody:
Fish:
Anatomical Terms:
Stage Range: Days 21-29 to Days 45-89
PHENOTYPE:
Fish:
Observed In:
Stage Range: Days 21-29 to Days 45-89

Fig. 5

vclb deficiency causes disorganization of coronary vessels. The Tg(fli1a:EGFP) transgenic line (endothelial cells labeled by EGFP) is used to trace coronary vessel development. The Tg(tcf21:dsRed) transgenic line is used to label epicardial cells. (A-H) In wild-type hearts, coronary vessels first appear on the dorsal surface of the ventricle and are close to the atrium-ventricle connection at ~28 dpf. Coronary vessels then spread, extend, and wrap the entire ventricle wall from 35 to 55 dpf. Dorsal views (A-D) and ventral views (E-H) are shown. (I-P) In the v12 mutant, coronary vessels appear at the same place as in wild-type siblings, but more vessels are detected at the initial stages. Wild-type coronary vessels are well connected to each other, but the overproliferated mutant vessels remain isolated and disorganized. Dorsal views (I-L) and ventral views (M-P) are shown. (Q-R') In the v12 mutant, coronary vessels are surrounded by epicardial-derived cells (R,R') rather than by cardiac muscles as in the wild-type sibling (Q,Q') at 55 dpf. MF20 stains cardiac muscles. Arrows indicate vessels that are (Q,Q') or are not (R,R') in contact with cardiac muscle. (S-V'') At 40 dpf, Tg(fli1:EGFP)-labeled endothelial tubes in wild-type ventricles are well aligned with Tg(tcf21:dsRed)-labeled epicardial-derived perivascular cells (S,S',U-U''). By contrast, most of the endothelial tubes in v12 mutants are not well aligned with perivascular cells (T,T',V-V''). Note the overproliferated endothelial and perivascular cells in the mutant. Results are shown in whole-mount view (S-T') and cryosection (U-V''). Scale bars: 100 μm in A-P; 10 μm in Q-R′; 20 μm in S-V″.

Gene Expression Details
Gene Antibody Fish Conditions Stage Anatomy Assay
DsRed2 vclbgd4Gt/gd4Gt; pd37Tg; y1Tg standard conditions Days 30-44 epicardium IHC
Days 30-44 heart vasculature anatomical region IHC
y1Tg ; pd37Tg standard conditions Days 30-44 epicardium IHC
Days 30-44 heart vasculature anatomical region IHC
EGFP vclbgd4Gt/gd4Gt; pd37Tg; y1Tg standard conditions Days 30-44 heart vasculature endothelial cell IHC
vclbgd4Gt/gd4Gt; y1Tg standard conditions Days 21-29 heart vasculature IFL
Days 30-44 heart vasculature IFL
Days 45-89 heart vasculature IFL
Days 45-89 heart vasculature endothelial cell IHC
y1Tg standard conditions Days 21-29 heart vasculature IFL
Days 30-44 heart vasculature IFL
Days 45-89 heart vasculature IFL
Days 45-89 heart vasculature endothelial cell IHC
y1Tg ; pd37Tg standard conditions Days 30-44 heart vasculature endothelial cell IHC
Antibody Labeling Details
Antibody Assay Fish Conditions Stage Anatomy
Ab-MF20 IHC vclbgd4Gt/gd4Gt; y1Tg standard conditions Days 45-89 myocardium
IHC y1Tg standard conditions Days 45-89 myocardium
Phenotype Details
Fish Conditions Stage Phenotype
vclbgd4Gt/gd4Gt; pd37Tg; y1Tg standard conditions Days 30-44 epicardium cell increased accumulation heart vasculature anatomical region, abnormal
Days 30-44 heart vasculature blood vessel increased amount, abnormal
vclbgd4Gt/gd4Gt; y1Tg standard conditions Days 21-29 heart vasculature blood vessel disorganized, abnormal
Days 21-29 heart vasculature blood vessel increased amount, abnormal
Days 30-44 heart vasculature blood vessel disorganized, abnormal
Days 30-44 heart vasculature blood vessel increased amount, abnormal
Days 45-89 heart vasculature blood vessel disorganized, abnormal
Days 45-89 heart vasculature blood vessel increased amount, abnormal
Acknowledgments:
ZFIN wishes to thank the journal Development (Cambridge, England) for permission to reproduce figures from this article. Please note that this material may be protected by copyright. Full text @ Development