Phenotype
|
Fish
|
Conditions
|
Figures
|
pharyngeal endoderm mislocalised laterally, abnormal
|
AB + MO1-s1pr2
|
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
|
AB + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Fukui et al., 2014
|
myocardial precursor mislocalised laterally, abnormal
|
AB + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Fukui et al., 2014
|
heart tube split bilaterally, abnormal
|
AB + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Fukui et al., 2014
|
embryonic heart tube morphogenesis disrupted, abnormal
|
AB/TU + MO1-s1pr2
|
standard conditions
|
Fig. 3
from Nakanaga et al., 2014
|
prechordal plate increased width, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Kai et al., 2008
|
pericardium edematous, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Ye et al., 2013
|
heart bifurcated, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. S4,
Fig. S11
from Kawahara et al., 2009
|
epidermal cell cell aggregation decreased amount, abnormal
|
WT + MO1-s1pr2
|
chemical treatment: EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
|
Fig. 7
from Gu et al., 2015
|
posterior lateral line has fewer parts of type posterior lateral line neuromast, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 3
from Hu et al., 2013
|
semicircular canal broken into two pieces, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Hu et al., 2013
|
hypoblast mesodermal cell spatial pattern, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. S4
from Kai et al., 2008
|
utricle increased size, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Hu et al., 2013
|
neuromast hair cell apoptotic, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 5
from Hu et al., 2013
|
pharyngeal arch 1 morphology, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. S1
from Hisano et al., 2013
|
heart tube bifurcated, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. S3
from Hisano et al., 2013
|
posterior lateral line neuromast hair cell development disrupted, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 3
from Hu et al., 2013
|
heart duplicated, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Ye et al., 2013
|
semicircular canal development disrupted, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Hu et al., 2013
|
anterior lateral line neuromast hair cell development disrupted, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 3
from Hu et al., 2013
|
posterior lateral line neuromast decreased size, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 3
from Hu et al., 2013
|
cell migration involved in gastrulation disrupted, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 1 ,
Fig. S3
from Kai et al., 2008
|
pharyngeal arch 1 decreased length, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. S1
from Hisano et al., 2013
|
epidermal cell aggregated, abnormal
|
WT + MO1-s1pr2
|
control
|
Fig. 7
from Gu et al., 2015
|
semicircular canal morphology, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Hu et al., 2013
|
prechordal plate flat, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Kai et al., 2008
|
otic vesicle morphogenesis disrupted, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Hu et al., 2013
|
caudal fin blistered, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Ye et al., 2013
Fig. S4
from Kawahara et al., 2009
|
otolith malformed, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Hu et al., 2013
|
anterior lateral line neuromast hair cell decreased amount, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 3
from Hu et al., 2013
|
mesodermal cell migration increased rate, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Kai et al., 2008
|
neural keel increased length, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. S3
from Kai et al., 2008
|
otolith increased size, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Hu et al., 2013
|
saccule decreased size, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Hu et al., 2013
|
prechordal plate increased length, abnormal
|
WT + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Kai et al., 2008
|
heart tube split bilaterally, abnormal
|
ha01Tg + MO1-s1pr2
|
standard conditions
|
Fig. 3
from Fukui et al., 2014
|
cardiac muscle progenitor cell migration to the midline involved in heart field formation decreased occurrence, abnormal
|
ha01Tg + MO1-s1pr2
|
standard conditions
|
Fig. 3
from Fukui et al., 2014
|
endoderm anterior region apoptotic, abnormal
|
ha01Tg + MO1-s1pr2
|
standard conditions
|
Fig. 3
from Fukui et al., 2014
|
heart morphogenesis decreased process quality, abnormal
|
ha01Tg + MO1-s1pr2
|
standard conditions
|
Fig. 3
from Fukui et al., 2014
|
endoderm apoptotic process increased occurrence, abnormal
|
ha01Tg + MO1-s1pr2
|
standard conditions
|
Fig. 3
from Fukui et al., 2014
|
heart tube increased amount, abnormal
|
ko07Tg + MO1-s1pr2
|
standard conditions
|
Fig. S1
from Hisano et al., 2013
|
heart tube mislocalised laterally, abnormal
|
ko07Tg + MO1-s1pr2
|
standard conditions
|
Fig. S1
from Hisano et al., 2013
|
heart bifurcated, abnormal
|
ko07Tg + MO1-s1pr2
|
standard conditions
|
Fig. S4
from Kawahara et al., 2009
|
cardioblast migration to the midline involved in heart rudiment formation disrupted, abnormal
|
ko07Tg + MO1-s1pr2
|
standard conditions
|
Fig. S1
from Hisano et al., 2013
|
cardioblast migration to the midline involved in heart rudiment formation decreased process quality, abnormal
|
ko07Tg + MO1-s1pr2
|
standard conditions
|
Fig. S1
from Hisano et al., 2013
|
heart split bilaterally, abnormal
|
ncv10Tg + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Fukui et al., 2014
|
heart malformed, abnormal
|
ncv10Tg + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Fukui et al., 2014
|
heart morphogenesis decreased process quality, abnormal
|
ncv10Tg + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Fukui et al., 2014
|
heart duplicated, abnormal
|
twu34Tg + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Ye et al., 2013
|
myocardial precursor mislocalised laterally, abnormal
|
ha01Tg; ncv11Tg + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Fukui et al., 2014
|
heart morphogenesis decreased process quality, abnormal
|
ha01Tg; ncv11Tg + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Fukui et al., 2014
|
endoderm antero-medial region decreased object quality, abnormal
|
ha01Tg; ncv11Tg + MO1-s1pr2
|
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-s1pr2
|
standard conditions
|
Fig. 2
from Fukui et al., 2014
|
heart tube split bilaterally, abnormal
|
ha01Tg; ncv11Tg + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Fukui et al., 2014
|
heart duplicated, abnormal
|
ha01Tg; twu34Tg + MO1-s1pr2
|
standard conditions
|
Fig. 7
from Ye et al., 2013
|
endoderm anterior region perforate, abnormal
|
ha01Tg; twu34Tg + MO1-s1pr2
|
standard conditions
|
Fig. 7
from Ye et al., 2013
|
endoderm anterior region increased width, abnormal
|
ha01Tg; twu34Tg + MO1-s1pr2
|
standard conditions
|
Fig. 7
from Ye et al., 2013
|
endocardium mislocalised, abnormal
|
is5Tg; ui6Tg + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Xie et al., 2016
|
pharyngeal arch 1 decreased length, abnormal
|
fn1akt259/kt259 + MO1-s1pr2
|
standard conditions
|
Fig. S1
from Hisano et al., 2013
|
pharyngeal arch 1 morphology, abnormal
|
fn1akt259/kt259 + MO1-s1pr2
|
standard conditions
|
Fig. S1
from Hisano et al., 2013
|
heart bifurcated, abnormal
|
spns2ko157/ko157 + MO1-s1pr2
|
standard conditions
|
Fig. S11
from Kawahara et al., 2009
|
involution involved in gastrulation with mouth forming second disrupted, abnormal
|
wnt11f2tx226/tx226 + MO1-s1pr2
|
standard conditions
|
Fig. 4
from Kai et al., 2008
|
mesodermal cell lamellipodium increased length, abnormal
|
wnt11f2tx226/tx226 + MO1-s1pr2
|
standard conditions
|
Fig. 3
from Kai et al., 2008
|
mesodermal cell migration process quality, abnormal
|
wnt11f2tx226/tx226 + MO1-s1pr2
|
standard conditions
|
Fig. 3
from Kai et al., 2008
|
hypoblast mesodermal cell cellular motility, abnormal
|
wnt11f2tx226/tx226 + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Kai et al., 2008
|
notochord decreased length, abnormal
|
wnt11f2tx226/tx226 + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Kai et al., 2008
|
hypoblast mesodermal cell spatial pattern, abnormal
|
wnt11f2tx226/tx226 + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Kai et al., 2008
|
notochord increased thickness, abnormal
|
wnt11f2tx226/tx226 + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Kai et al., 2008
|
hypoblast mesodermal cell increased speed, abnormal
|
wnt11f2tx226/tx226 + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Kai et al., 2008
|
cell migration involved in gastrulation disrupted, abnormal
|
wnt11f2tx226/tx226 + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Kai et al., 2008
|
convergent extension involved in gastrulation disrupted, abnormal
|
wnt11f2tx226/tx226 + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Kai et al., 2008
|
prechordal plate increased length, abnormal
|
wnt11f2tx226/tx226 + MO1-s1pr2
|
standard conditions
|
Fig. 1
from Kai et al., 2008
|
mesodermal cell migration persistence, abnormal
|
wnt11f2tx226/tx226 + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Kai et al., 2008
|
intersegmental vessel shortened, abnormal
|
y1Tg + MO1-s1pr2 + MO2-s1pr1
|
standard conditions
|
Fig. 7
from Mendelson et al., 2013
|
intersegmental vessel morphology, abnormal
|
y1Tg + MO1-s1pr2 + MO2-s1pr1
|
standard conditions
|
Fig. 7
from Mendelson et al., 2013
|
heart tube increased amount, abnormal
|
fn1akt259/kt259; ko07Tg + MO1-s1pr2
|
standard conditions
|
Fig. S1
from Hisano et al., 2013
|
cardioblast migration to the midline involved in heart rudiment formation absent, abnormal
|
fn1akt259/kt259; ko07Tg + MO1-s1pr2
|
standard conditions
|
Fig. S1
from Hisano et al., 2013
|
cardioblast migration to the midline involved in heart rudiment formation disrupted, abnormal
|
fn1akt259/kt259; ko07Tg + MO1-s1pr2
|
standard conditions
|
Fig. S1
from Hisano et al., 2013
|
heart tube mislocalised laterally, abnormal
|
fn1akt259/kt259; ko07Tg + MO1-s1pr2
|
standard conditions
|
Fig. S1
from Hisano et al., 2013
|
heart bifurcated, abnormal
|
spns2ko157/+; ko07Tg + MO1-s1pr2
|
standard conditions
|
Fig. 2
from Kawahara et al., 2009
|