| Phenotype | Fish | Conditions | Figures | 
    
    
        
            | heart edematous, abnormal | WT + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. S2  from Rydeen et al., 2014 
 | 
    
        
            | hindbrain edematous, abnormal | WT + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. S2  from Rydeen et al., 2014 
 | 
    
        
            | whole organism mmp9 expression increased amount, abnormal | WT + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. 5  from Rydeen et al., 2016 
 | 
    
        
            | whole organism fgf8a expression decreased amount, abnormal | WT + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. 4  from Rydeen et al., 2016 
 | 
    
        
            | heart fgf8a expression decreased amount, abnormal | WT + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. 4  from Rydeen et al., 2016 
 | 
    
        
            | heart mmp9 expression increased amount, abnormal | WT + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. 5  from Rydeen et al., 2016 
 | 
    
        
            | hindbrain edematous, abnormal | WT + MO1-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. S2  from Rydeen et al., 2014 
 | 
    
        
            | atrium has fewer parts of type cardiac muscle cell, abnormal | WT + MO1-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. 2  from Rydeen et al., 2014 
 | 
    
        
            | heart edematous, abnormal | WT + MO1-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. S2  from Rydeen et al., 2014 
 | 
    
        
            | midbrain hindbrain boundary absent, abnormal | WT + MO2-rarab + MO4-cyp26a1 + MO4-tp53 + MO5-cyp26a1 | standard conditions | Fig. 5  , 
                    
                        Fig. 6  from D'Aniello et al., 2013 
 | 
    
        
            | caudal fin shortened, abnormal | WT + MO2-rarab + MO4-cyp26a1 + MO4-tp53 + MO5-cyp26a1 | standard conditions | Fig. 5  from D'Aniello et al., 2013 
 | 
    
        
            | ventricular myocardium cardiac muscle cell mislocalised, abnormal | f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | heat shock | Fig. 4  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle has fewer parts of type cardiac muscle cell, abnormal | f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 5  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle has number of cardiac muscle cell, ameliorated | f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | chemical treatment by environment: 3-(N-HYDROXYCARBOXAMIDO)-2-ISOBUTYLPROPANOYL-TRP-METHYLAMIDE | Fig. 5  from Rydeen et al., 2016 
 | 
    
        
            | whole organism myl7 expression decreased amount, abnormal | f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. 1  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle has fewer parts of type cardiac muscle cell, abnormal | f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | heat shock | Fig. 4  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle cardiac ventricle morphogenesis decreased process quality, abnormal | f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 1  , 
                    
                        Fig. 5  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle decreased size, abnormal | f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. 1  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle cardiac ventricle morphogenesis decreased process quality, abnormal | f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | heat shock | Fig. 4  from Rydeen et al., 2016 
 | 
    
        
            | cardiac muscle cell external to heart, abnormal | f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | heat shock | Fig. 4  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle cardiac ventricle morphogenesis process quality, ameliorated | f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | chemical treatment by environment: 3-(N-HYDROXYCARBOXAMIDO)-2-ISOBUTYLPROPANOYL-TRP-METHYLAMIDE | Fig. 5  from Rydeen et al., 2016 
 | 
    
        
            | whole organism myh7 expression decreased amount, abnormal | f2Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. 1  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle has fewer parts of type cardiac muscle cell, abnormal | f2Tg + MO2-rarab + MO4-cyp26a1 + MO4-tp53 + MO5-cyp26a1 | standard conditions | Fig. 5  from D'Aniello et al., 2013 
 | 
    
        
            | heart has fewer parts of type cardiac muscle cell, abnormal | f2Tg + MO2-rarab + MO4-cyp26a1 + MO4-tp53 + MO5-cyp26a1 | standard conditions | Fig. 5  from D'Aniello et al., 2013 
 | 
    
        
            | presumptive bulbus arteriosus ripply3 expression increased amount, abnormal | fb7Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO4-tp53 + MO5-cyp26a1 | standard conditions | Fig 7  from Song et al., 2019 
 | 
    
        
            | cell migration involved in heart formation process quality, abnormal | fb7Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. 2  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle cell migration involved in heart formation decreased process quality, abnormal | fb9Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 2  from Rydeen et al., 2016 
 | 
    
        
            | aortic arch has extra parts of type blood vessel endothelial cell, abnormal | fb9Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 2  from Rydeen et al., 2016 
 | 
    
        
            | bulbus arteriosus outflow tract morphogenesis decreased process quality, abnormal | sd22Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | heat shock | Fig. 4  from Rydeen et al., 2016 
 | 
    
        
            | bulbus arteriosus outflow tract morphogenesis process quality, ameliorated | sd22Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | chemical treatment by environment: 3-(N-HYDROXYCARBOXAMIDO)-2-ISOBUTYLPROPANOYL-TRP-METHYLAMIDE | Fig. 5  from Rydeen et al., 2016 
 | 
    
        
            | cardiac muscle cell external to heart, abnormal | sd22Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. 1  from Rydeen et al., 2016 
 | 
    
        
            | cardiac muscle cell mislocalised, abnormal | sd22Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. 1  from Rydeen et al., 2016 
 | 
    
        
            | bulbus arteriosus outflow tract morphogenesis decreased process quality, abnormal | sd22Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. 1  , 
                    
                        Fig. 5  from Rydeen et al., 2016 
 | 
    
        
            | ventricular myocardium cardiac muscle cell mislocalised, abnormal | twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 3  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle cardiac ventricle morphogenesis decreased process quality, abnormal | twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 3  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle cardiac muscle cell circular, abnormal | twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 3  from Rydeen et al., 2016 
 | 
    
        
            | ventricular myocardium cell-cell junction ab1-ctnnb labeling spatial pattern, abnormal | twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 3  from Rydeen et al., 2016 
 | 
    
        
            | ventricular myocardium bicellular tight junction ab1-tjp1 labeling spatial pattern, abnormal | twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 3  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle establishment of cell polarity decreased process quality, abnormal | twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 3  from Rydeen et al., 2016 
 | 
    
        
            | endocardium has fewer parts of type endothelial cell, abnormal | ubs1Tg + MO1-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. 7  from Rydeen et al., 2014 
 | 
    
        
            | cranial vasculature has fewer parts of type endothelial cell, abnormal | ubs1Tg + MO1-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | standard conditions | Fig. 7  from Rydeen et al., 2014 
 | 
    
        
            | ventricular myocardium increased distance ventricular endocardium, abnormal | ci5Tg; twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 3  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle cardiac ventricle morphogenesis decreased process quality, abnormal | ci5Tg; twu34Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 3  from Rydeen et al., 2016 
 | 
    
        
            | aortic arch 4 has extra parts of type blood vessel endothelial cell, abnormal | fb9Tg; ubs1Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 2  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle cell migration involved in heart formation decreased process quality, abnormal | fb9Tg; ubs1Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 2  from Rydeen et al., 2016 
 | 
    
        
            | aortic arch 3 has extra parts of type blood vessel endothelial cell, abnormal | fb9Tg; ubs1Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | control | Fig. 2  from Rydeen et al., 2016 
 | 
    
        
            | ventricular myocardium cardiac muscle cell mislocalised, abnormal | f2Tg; pd3Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | heat shock | Fig. 4  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle has fewer parts of type cardiac muscle cell, abnormal | f2Tg; pd3Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | heat shock | Fig. 4  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle has number of cardiac muscle cell, ameliorated | f2Tg; pd3Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | heat shock | Fig. 4  from Rydeen et al., 2016 
 | 
    
        
            | cardiac muscle cell external to heart, abnormal | f2Tg; pd3Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | heat shock | Fig. 4  from Rydeen et al., 2016 
 | 
    
        
            | cardiac ventricle cardiac ventricle morphogenesis decreased process quality, abnormal | f2Tg; pd3Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | heat shock | Fig. 4  from Rydeen et al., 2016 
 | 
    
        
            | bulbus arteriosus outflow tract morphogenesis process quality, ameliorated | pd3Tg; sd22Tg + MO1-cyp26c1 + MO2-cyp26c1 + MO4-cyp26a1 + MO5-cyp26a1 | heat shock | Fig. 4  from Rydeen et al., 2016 
 |