Phenotype
|
Fish
|
Conditions
|
Figures
|
pronephric glomerulus lacks all parts of type pronephric glomerular capillary, abnormal
|
AB + MO2-foxc1a
|
standard conditions
|
Fig. 4
from He et al., 2014
|
pronephric podocyte cell projection malformed, abnormal
|
AB + MO2-foxc1a
|
standard conditions
|
Fig. 4
from He et al., 2014
|
podocyte development decreased process quality, abnormal
|
AB + MO2-foxc1a
|
standard conditions
|
Fig. 4
from He et al., 2014
|
pronephric glomerulus lacks all parts of type pronephric podocyte slit diaphragm, abnormal
|
AB + MO2-foxc1a
|
standard conditions
|
Fig. 4
from He et al., 2014
|
closure of optic fissure arrested, abnormal
|
WT + MO1-foxc1a + MO2-foxc1a
|
standard conditions
|
Fig. 6
from Lupo et al., 2011
|
optic fissure closure incomplete, abnormal
|
WT + MO1-foxc1a + MO2-foxc1a
|
standard conditions
|
Fig. 6
from Lupo et al., 2011
|
pericardium edematous, abnormal
|
WT + MO2-foxc1a
|
standard conditions
|
Fig. 2
from Skarie et al., 2009
|
somitogenesis process quality, abnormal
|
WT + MO2-foxc1a
|
standard conditions
|
Fig. 3
from Li et al., 2015
|
eye hemorrhagic, abnormal
|
WT + MO2-foxc1a
|
standard conditions
|
Fig. 2
from Skarie et al., 2009
|
brain hydrocephalic, abnormal
|
WT + MO2-foxc1a
|
standard conditions
|
Fig. 2
from Skarie et al., 2009
|
eye decreased size, abnormal
|
WT + MO2-foxc1a
|
standard conditions
|
Fig. 2
from Skarie et al., 2009
|
central nervous system hemorrhagic, abnormal
|
WT + MO2-foxc1a
|
standard conditions
|
Fig. 2
from Skarie et al., 2009
|
pronephric glomerulus physical object quality, abnormal
|
ki1Tg + MO2-foxc1a
|
standard conditions
|
Fig. 3
from He et al., 2014
|
heart edematous, abnormal
|
ki1Tg + MO2-foxc1a
|
standard conditions
|
Fig. 3
from He et al., 2014
|
vasculature development disrupted, abnormal
|
s843Tg; sd2Tg + MO2-foxc1a
|
standard conditions
|
Fig. 4
from De Val et al., 2008
|
blood circulation disrupted, abnormal
|
s843Tg; sd2Tg + MO2-foxc1a
|
standard conditions
|
Fig. 4
from De Val et al., 2008
|
intersegmental vessel decreased amount, abnormal
|
s843Tg; sd2Tg + MO2-foxc1a
|
standard conditions
|
Fig. 4
from De Val et al., 2008
|
neural crest pdgfra expression decreased amount, abnormal
|
foxc1bua1018/ua1018 + MO2-foxc1a (AB)
|
standard conditions
|
Fig. S2
from Umali et al., 2019
|
solid lens vesicle pdgfra expression decreased amount, abnormal
|
foxc1bua1018/ua1018 + MO2-foxc1a (AB)
|
standard conditions
|
Fig. S2
from Umali et al., 2019
|
retinal ganglion cell layer pou4f2 expression decreased amount, abnormal
|
foxc1bua1018/ua1018 + MO2-foxc1a (AB)
|
standard conditions
|
Fig. 4
from Umali et al., 2019
|
retina atoh7 expression absent, abnormal
|
foxc1bua1018/ua1018 + MO2-foxc1a (AB)
|
standard conditions
|
Fig. 4
from Umali et al., 2019
|
cranial nerve II decreased diameter, abnormal
|
foxc1bua1018/ua1018 + MO2-foxc1a (AB)
|
standard conditions
|
Fig. 3
from Umali et al., 2019
|
retina atoh7 expression decreased amount, abnormal
|
foxc1bua1018/ua1018 + MO2-foxc1a (AB)
|
standard conditions
|
Fig. 4
from Umali et al., 2019
|
pharyngeal arch pdgfra expression decreased amount, abnormal
|
foxc1bua1018/ua1018 + MO2-foxc1a (AB)
|
standard conditions
|
Fig. S2
from Umali et al., 2019
|
retinal ganglion cell neuron differentiation decreased occurrence, abnormal
|
foxc1bua1018/ua1018 + MO2-foxc1a (AB)
|
standard conditions
|
Fig. 4
from Umali et al., 2019
|
retinal ganglion cell layer has fewer parts of type retinal ganglion cell, abnormal
|
foxc1bua1018/ua1018 + MO2-foxc1a (AB)
|
standard conditions
|
Fig. 2
from Umali et al., 2019
|
head fgf19 expression decreased amount, abnormal
|
foxc1bua1018/ua1018 + MO2-foxc1a (AB)
|
standard conditions
|
Fig. 5
from Umali et al., 2019
|
retina layer formation delayed, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 3
from Skarie et al., 2009
|
brain vasculature morphology, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. S2
from French et al., 2014
|
lens development in camera-type eye delayed, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 3
from Skarie et al., 2009
|
pericardium edematous, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 2
from Skarie et al., 2009
|
periocular mesenchyme disorganized, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 3
from Skarie et al., 2009
|
eye hemorrhagic, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 2,
Fig. 8
from Skarie et al., 2009
|
blood circulation disrupted, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 2
from Skarie et al., 2009
|
hyaloid vessel decreased amount, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 3
from Skarie et al., 2009
|
eye decreased size, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 2,
Fig. 3
from Skarie et al., 2009
|
corneal stroma structure, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 3
from Skarie et al., 2009
|
central nervous system hemorrhagic, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 2,
Fig. 8
from Skarie et al., 2009
|
eye basement membrane disorganized, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 6
from Skarie et al., 2009
|
eye hemorrhagic, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
chemical treatment: N-phenylthiourea
|
Fig. 7
from Acharya et al., 2011
|
eye apoptotic, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 7
from Berry et al., 2008
|
hyaloid vessel dilated, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 3
from Skarie et al., 2009
|
ventricular system distended, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 3
from Skarie et al., 2009
|
eye basement membrane morphology, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 7
from Skarie et al., 2009
|
brain hydrocephalic, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
chemical treatment: N-phenylthiourea
|
Fig. 7
from Acharya et al., 2011
|
whole organism decreased length, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
chemical treatment: N-phenylthiourea
|
Fig. 7
from Acharya et al., 2011
|
neural crest cell migration delayed, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. S4
from French et al., 2014
|
brain hemorrhagic, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 1,
Fig. 2
from French et al., 2014
|
hyaloid vessel morphology, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 6
from Skarie et al., 2009
|
brain hydrocephalic, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 2,
Fig. 8
from Skarie et al., 2009
|
corneal endothelium aplastic, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 3
from Skarie et al., 2009
|
central nervous system hemorrhagic, abnormal
|
sd2Tg/+ + MO1-foxc1b + MO1-pawr + MO2-foxc1a
|
chemical treatment: N-phenylthiourea
|
Fig. 8
from Acharya et al., 2011
|
eye hemorrhagic, abnormal
|
sd2Tg/+ + MO1-foxc1b + MO1-pawr + MO2-foxc1a
|
chemical treatment: N-phenylthiourea
|
Fig. 8
from Acharya et al., 2011
|
brain hydrocephalic, abnormal
|
WT + MO1-foxc1b + MO1-pawr + MO2-foxc1a
|
chemical treatment: N-phenylthiourea
|
Fig. 8
from Acharya et al., 2011
|
central nervous system hemorrhagic, abnormal
|
WT + MO1-foxc1b + MO1-pawr + MO2-foxc1a
|
chemical treatment: N-phenylthiourea
|
Fig. 8
from Acharya et al., 2011
|
brain hemorrhagic, abnormal
|
WT + MO1-foxc1b + MO1-pdgfrb + MO2-foxc1a
|
standard conditions
|
Fig. 2
from French et al., 2014
|
brain hemorrhagic, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a + MO2-pdgfra
|
standard conditions
|
Fig. 2
from French et al., 2014
|
central nervous system hemorrhagic, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a + MO5-lama1
|
standard conditions
|
Fig. 8
from Skarie et al., 2009
|
eye hemorrhagic, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a + MO5-lama1
|
standard conditions
|
Fig. 8
from Skarie et al., 2009
|
brain hydrocephalic, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a + MO5-lama1
|
standard conditions
|
Fig. 8
from Skarie et al., 2009
|
whole organism decreased length, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a + MO7-pitx2
|
chemical treatment: N-phenylthiourea
|
Fig. 8
from Acharya et al., 2011
|
brain hydrocephalic, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a + MO7-pitx2
|
chemical treatment: N-phenylthiourea
|
Fig. 8
from Acharya et al., 2011
|
pericardium edematous, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a + MO7-pitx2
|
chemical treatment: N-phenylthiourea
|
Fig. 8
from Acharya et al., 2011
|
brain decreased size, abnormal
|
WT + MO1-foxc1b + MO2-foxc1a + MO7-pitx2
|
chemical treatment: N-phenylthiourea
|
Fig. 8
from Acharya et al., 2011
|
brain hemorrhagic, abnormal
|
WT + MO1-foxc1b + MO1-pdgfrb + MO2-foxc1a + MO2-pdgfra
|
standard conditions
|
Fig. 2
from French et al., 2014
|
pronephric glomerulus physical object quality, abnormal
|
ki1Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 3
from He et al., 2014
|
heart edematous, abnormal
|
ki1Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 3
from He et al., 2014
|
pronephric glomerulus physical object quality, abnormal
|
ki1Tg + MO1-lmx1bb + MO2-foxc1a
|
standard conditions
|
Fig. 3
from He et al., 2014
|
heart edematous, abnormal
|
ki1Tg + MO1-lmx1bb + MO2-foxc1a
|
standard conditions
|
Fig. 3
from He et al., 2014
|
intersegmental vessel increased branchiness, abnormal
|
y5Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 5
from Skarie et al., 2009
|
dorsal aorta morphology, abnormal
|
y5Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 4
from Skarie et al., 2009
|
hyaloid vessel blood vessel endothelial cell disorganized, abnormal
|
y5Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 4
from Skarie et al., 2009
|
cardinal system morphology, abnormal
|
y5Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 4
from Skarie et al., 2009
|
vasculature broken, abnormal
|
y5Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 4
from Skarie et al., 2009
|
blood vessel endothelial cell disorganized, abnormal
|
y5Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 5
from Skarie et al., 2009
|
central nervous system hemorrhagic, abnormal
|
y5Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 4,
Fig. 5
from Skarie et al., 2009
|
hyaloid vessel dilated, abnormal
|
y5Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 4
from Skarie et al., 2009
|
eye hemorrhagic, abnormal
|
y5Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 4,
Fig. 5
from Skarie et al., 2009
|
hyaloid vessel branchiness, abnormal
|
y5Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 4
from Skarie et al., 2009
|
neural crest cell migration disrupted, abnormal
|
zf15Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 3
from Skarie et al., 2009
|
eye decreased size, abnormal
|
zf15Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 3
from Skarie et al., 2009
|
cerebellum vascular associated smooth muscle cell decreased amount, abnormal
|
ca7Tg; ci5Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 3
from French et al., 2014
|
brain vasculature neural crest cell decreased amount, abnormal
|
ci5Tg; zf566Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 3
from French et al., 2014
|
axial vasculature decreased size, abnormal
|
s843Tg; sd2Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 4
from De Val et al., 2008
|
intersegmental vessel aplastic, abnormal
|
s843Tg; sd2Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 4
from De Val et al., 2008
|
blood circulation disrupted, abnormal
|
s843Tg; sd2Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 4
from De Val et al., 2008
|
vasculature development disrupted, abnormal
|
s843Tg; sd2Tg + MO1-foxc1b + MO2-foxc1a
|
standard conditions
|
Fig. 4
from De Val et al., 2008
|
blood circulation disrupted, abnormal
|
s843Tg; sd2Tg + MO2-foxc1a + MO3-etsrp
|
standard conditions
|
Fig. 4
from De Val et al., 2008
|
vasculature development disrupted, abnormal
|
s843Tg; sd2Tg + MO2-foxc1a + MO3-etsrp
|
standard conditions
|
Fig. 4
from De Val et al., 2008
|