Phenotype
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Fish
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Conditions
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Figures
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caudal fin blistered, abnormal
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WT + MO1-gna13a + MO1-gna13b
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standard conditions
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Fig. 1
from Ye et al., 2013
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pericardium edematous, abnormal
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WT + MO1-gna13a + MO1-gna13b
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standard conditions
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Fig. 1
from Ye et al., 2013
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myocardium unfused from myocardium, abnormal
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WT + MO1-gna13a + MO1-gna13b
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standard conditions
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Fig. 8
from Xie et al., 2016
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endocardium unfused from endocardium, abnormal
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WT + MO1-gna13a + MO1-gna13b
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standard conditions
|
Fig. 1
from Xie et al., 2016
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heart duplicated, abnormal
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WT + MO1-gna13a + MO1-gna13b
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standard conditions
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Fig. S1
from Ye et al., 2013
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endothelial cell absent, abnormal
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WT + MO1-etsrp + MO1-gna13a + MO1-gna13b + MO2-etsrp
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standard conditions
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Fig. 8
from Xie et al., 2016
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endothelial cell cdh5 expression absent, abnormal
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WT + MO1-etsrp + MO1-gna13a + MO1-gna13b + MO2-etsrp
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standard conditions
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Fig. 8
from Xie et al., 2016
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myocardium fused with myocardium, ameliorated
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WT + MO1-etsrp + MO1-gna13a + MO1-gna13b + MO2-etsrp
|
standard conditions
|
Fig. 8
from Xie et al., 2016
|
myocardial precursor cardioblast migration to the midline involved in heart field formation occurrence, ameliorated
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WT + MO1-etsrp + MO1-gna13a + MO1-gna13b + MO2-etsrp
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standard conditions
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Fig. 8
from Xie et al., 2016
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epiboly involved in gastrulation with mouth forming second disrupted, abnormal
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WT + MO1-gna12a + MO1-gna13a + MO1-gna13b
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standard conditions
|
Fig. 1,
Fig. 6
from Lin et al., 2009
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heart duplicated, abnormal
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WT + MO1-gna12a + MO1-gna13a + MO1-gna13b
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standard conditions
|
Fig. S1
from Ye et al., 2013
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myelination of posterior lateral line nerve axons disrupted, abnormal
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WT + MO1-gna12a + MO1-gna13a + MO1-gna13b
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standard conditions
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Fig. 3
from Ackerman et al., 2018
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myelination of posterior lateral line nerve axons disrupted, abnormal
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adgrg1stl13/+ + MO1-gna12a + MO1-gna13a + MO1-gna13b
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standard conditions
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Fig. 3
from Ackerman et al., 2018
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spinal cord oligodendrocyte development decreased occurrence, abnormal
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adgrg1stl13/+ + MO1-gna12a + MO1-gna13a + MO1-gna13b (AB)
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standard conditions
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Fig. 7
from Ackerman et al., 2015
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myelination of posterior lateral line nerve axons disrupted, abnormal
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adgrg1stl13/stl13 + MO1-gna12a + MO1-gna13a + MO1-gna13b
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standard conditions
|
Fig. 3
from Ackerman et al., 2018
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spinal cord oligodendrocyte development decreased occurrence, abnormal
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adgrg1stl13/stl13 + MO1-gna12a + MO1-gna13a + MO1-gna13b (AB)
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standard conditions
|
Fig. 7
from Ackerman et al., 2015
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endoderm anterior region perforate, abnormal
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ha01Tg + MO1-gna13a + MO1-gna13b
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standard conditions
|
Fig. 5
from Ye et al., 2013
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endoderm anterior region increased width, abnormal
|
ha01Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 5
from Ye et al., 2013
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endocardium unfused from endocardium, abnormal
|
is1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 6
from Xie et al., 2016
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endocardium disorganized, abnormal
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is1Tg + MO1-gna13a + MO1-gna13b
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standard conditions
|
Fig. 6
from Xie et al., 2016
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endocardium structure, abnormal
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is1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 6
from Xie et al., 2016
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endocardium loose, abnormal
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is1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 6
from Xie et al., 2016
|
heart duplicated, abnormal
|
twu34Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 1 ,
Fig. S1
from Ye et al., 2013
|
heart duplicated, abnormal
|
twu34Tg + MO1-gna12a + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. S1
from Ye et al., 2013
|
myocardial precursor anatomical region ab2-fn labeling spatial pattern, abnormal
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fb7Tg; ui3Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 7
from Xie et al., 2016
|
endocardial precursor anatomical region ab2-fn labeling spatial pattern, abnormal
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fb7Tg; ui3Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 7
from Xie et al., 2016
|
endocardial progenitor cell migration to the midline involved in heart field formation decreased occurrence, abnormal
|
fb9Tg; y1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 2 ,
Fig. 8
from Xie et al., 2016
|
endocardial precursor cardioblast migration to the midline involved in heart field formation decreased occurrence, abnormal
|
fb9Tg; y1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 2 ,
Fig. 8
from Xie et al., 2016
|
endocardial precursor mislocalised, abnormal
|
fb9Tg; y1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 2
from Xie et al., 2016
|
myocardial precursor cardioblast migration to the midline involved in heart field formation decreased occurrence, abnormal
|
fb9Tg; y1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 2 ,
Fig. 8
from Xie et al., 2016
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endocardium cardioblast migration process quality, abnormal
|
fb9Tg; y1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 2
from Xie et al., 2016
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myocardial precursor mislocalised laterally, abnormal
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ha01Tg; ncv11Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 2
from Fukui et al., 2014
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heart tube split bilaterally, abnormal
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ha01Tg; ncv11Tg + MO1-gna13a + MO1-gna13b
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standard conditions
|
Fig. 2
from Fukui et al., 2014
|
heart morphogenesis decreased process quality, abnormal
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ha01Tg; ncv11Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 2
from Fukui et al., 2014
|
endoderm antero-medial region decreased object quality, abnormal
|
ha01Tg; ncv11Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 2
from Fukui et al., 2014
|
cardiac muscle progenitor cell migration to the midline involved in heart field formation decreased occurrence, abnormal
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ha01Tg; ncv11Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 2
from Fukui et al., 2014
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endoderm anterior region increased width, abnormal
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ha01Tg; twu34Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 7
from Ye et al., 2013
|
endoderm anterior region perforate, abnormal
|
ha01Tg; twu34Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 7
from Ye et al., 2013
|
heart duplicated, abnormal
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ha01Tg; twu34Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 7
from Ye et al., 2013
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endocardium mislocalised, abnormal
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is5Tg; ui6Tg + MO1-gna13a + MO1-gna13b
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standard conditions
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Fig. 1
from Xie et al., 2016
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endocardial precursor anatomical side ab2-fn labeling spatial pattern, abnormal
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ui3Tg; y1Tg + MO1-gna13a + MO1-gna13b
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standard conditions
|
Fig. 5
from Xie et al., 2016
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endocardial precursor fibronectin fibril disorganized, abnormal
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ui3Tg; y1Tg + MO1-gna13a + MO1-gna13b
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standard conditions
|
Fig. 5
from Xie et al., 2016
|
endocardial progenitor cell migration to the midline involved in heart field formation decreased occurrence, abnormal
|
ui3Tg; y1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 3
from Xie et al., 2016
|
endocardial precursor cardioblast migration to the midline involved in heart field formation decreased occurrence, abnormal
|
ui3Tg; y1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 3
from Xie et al., 2016
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endoderm cell migration process quality, abnormal
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ui3Tg; y1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 3
from Xie et al., 2016
|
endocardial precursor fibronectin fibril disoriented, abnormal
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ui3Tg; y1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 5
from Xie et al., 2016
|
endocardial precursor cell trailing edge ab2-fn labeling increased amount, abnormal
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ui3Tg; y1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 5
from Xie et al., 2016
|
endocardial precursor cell leading edge ab2-fn labeling decreased amount, abnormal
|
ui3Tg; y1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 5
from Xie et al., 2016
|
endoderm cell migration decreased occurrence, abnormal
|
ui3Tg; y1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 3
from Xie et al., 2016
|
endocardium cardioblast migration process quality, abnormal
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ui3Tg; y1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 4
from Xie et al., 2016
|
endocardial precursor fibronectin fibril organization decreased occurrence, abnormal
|
ui3Tg; y1Tg + MO1-gna13a + MO1-gna13b
|
standard conditions
|
Fig. 5
from Xie et al., 2016
|
endothelial cell absent, abnormal
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fb9Tg; y1Tg + MO1-etsrp + MO1-gna13a + MO1-gna13b + MO2-etsrp
|
standard conditions
|
Fig. 8
from Xie et al., 2016
|
endothelial cell EGFP expression absent, abnormal
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fb9Tg; y1Tg + MO1-etsrp + MO1-gna13a + MO1-gna13b + MO2-etsrp
|
standard conditions
|
Fig. 8
from Xie et al., 2016
|
myocardial precursor cardioblast migration to the midline involved in heart field formation occurrence, ameliorated
|
fb9Tg; y1Tg + MO1-etsrp + MO1-gna13a + MO1-gna13b + MO2-etsrp
|
standard conditions
|
Fig. 8
from Xie et al., 2016
|
endoderm antero-medial region decreased object quality, abnormal
|
ha01Tg; ncv11Tg + MO1-gna13a + MO1-gna13b + MO1-yap1 + MO3-ccn2a
|
standard conditions
|
Fig. 2
from Fukui et al., 2014
|
heart morphogenesis decreased process quality, abnormal
|
ha01Tg; ncv11Tg + MO1-gna13a + MO1-gna13b + MO1-yap1 + MO3-ccn2a
|
standard conditions
|
Fig. 2
from Fukui et al., 2014
|
heart tube split bilaterally, abnormal
|
ha01Tg; ncv11Tg + MO1-gna13a + MO1-gna13b + MO1-yap1 + MO3-ccn2a
|
standard conditions
|
Fig. 2
from Fukui et al., 2014
|
myocardial precursor mislocalised laterally, abnormal
|
ha01Tg; ncv11Tg + MO1-gna13a + MO1-gna13b + MO1-yap1 + MO3-ccn2a
|
standard conditions
|
Fig. 2
from Fukui et al., 2014
|
cardiac muscle progenitor cell migration to the midline involved in heart field formation decreased occurrence, abnormal
|
ha01Tg; ncv11Tg + MO1-gna13a + MO1-gna13b + MO1-yap1 + MO3-ccn2a
|
standard conditions
|
Fig. 2
from Fukui et al., 2014
|