Phenotype
|
Fish
|
Conditions
|
Figures
|
motor neuron axon truncated, abnormal
|
AB + MO1-smn1
|
standard conditions
|
Fig. S8,
Table S9
from Van Hoecke et al., 2012
Fig. 2
from McWhorter et al., 2003
|
motor neuron axon branched, abnormal
|
AB + MO1-smn1
|
standard conditions
|
Fig. 2
from McWhorter et al., 2003
|
cell Cajal body ab1-tmg labeling decreased amount, abnormal
|
AB + MO1-smn1
|
standard conditions
|
Fig. 8
from Strzelecka et al., 2010
|
cell small nuclear ribonucleoprotein complex dispersed, abnormal
|
AB + MO1-smn1
|
standard conditions
|
Fig. 8
from Strzelecka et al., 2010
|
CaP motoneuron axon decreased length, abnormal
|
AB + MO1-smn1
|
standard conditions
|
Fig. 1
from McWhorter et al., 2003
|
motor neuron axon increased branchiness, abnormal
|
AB + MO1-smn1
|
standard conditions
|
Table S9
from Van Hoecke et al., 2012
|
cell Cajal body ab1-coil labeling decreased amount, abnormal
|
AB + MO1-smn1
|
standard conditions
|
Fig. 8
from Strzelecka et al., 2010
|
whole organism smn1 expression decreased amount, abnormal
|
AB + MO1-smn1
|
standard conditions
|
Fig. 1
from Powis et al., 2016
|
CaP motoneuron morphology, abnormal
|
AB + MO1-smn1
|
standard conditions
|
Fig. 4
from McWhorter et al., 2008
|
cell Cajal body decreased amount, abnormal
|
AB + MO1-smn1
|
standard conditions
|
Fig. 8
from Strzelecka et al., 2010
|
whole organism Ab3-ub labeling decreased amount, abnormal
|
AB + MO1-smn1
|
standard conditions
|
Fig. 1
from Powis et al., 2016
|
CaP motoneuron axon increased branchiness, abnormal
|
AB + MO1-smn1
|
standard conditions
|
Fig. 1
from McWhorter et al., 2003
|
motor neuron axon truncated, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 5
from Winkler et al., 2005
|
ATP biosynthetic process decreased efficacy, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 2
from Boyd et al., 2017
|
primary motor neuron axon decreased length, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 5
from Boyd et al., 2017
|
motor neuron axon morphology, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 4
from Oprea et al., 2008
|
whole organism aerobic respiration decreased efficacy, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 2
from Boyd et al., 2017
|
motor neuron axon branchiness, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 5
from Winkler et al., 2005
|
whole organism Ab2-atp5a labeling decreased amount, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 2
from Boyd et al., 2017
|
CaP motoneuron axon decreased length, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 7
from Chitramuthu et al., 2010
|
primary motor neuron axon terminus swollen, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 5
from Boyd et al., 2017
|
axon extension process quality, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 7
from Chitramuthu et al., 2010
|
whole organism mitochondrion decreased functionality, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 2
from Boyd et al., 2017
|
mRNA splicing, via spliceosome decreased process quality, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 2
from See et al., 2014
|
CaP motoneuron axon branched, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 4
from See et al., 2014
Fig. 7
from Chitramuthu et al., 2010
|
axonogenesis disrupted, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 4
from Oprea et al., 2008
|
CaP motoneuron axon truncated, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 4
from See et al., 2014
|
primary motor neuron axonogenesis disrupted, abnormal
|
WT + MO1-smn1
|
standard conditions
|
Fig. 5
from Boyd et al., 2017
|
fast muscle cell synaptic cleft decreased width, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
CaP motoneuron axon decreased length, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
motor neuron axon morphology, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 1
from Powis et al., 2016
|
CaP motoneuron axon increased branchiness, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
axonogenesis disrupted, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 5
from Sleigh et al., 2014
|
motor neuron axon guidance disrupted, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 5
from Sleigh et al., 2014
|
primary motor neuron axon decreased length, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 3 ,
Fig. 6
from Boyd et al., 2017
|
swimming decreased rate, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. S3
from Riessland et al., 2017
|
primary motor neuron axonogenesis disrupted, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 3 ,
Fig. 6
from Boyd et al., 2017
|
CaP motoneuron axon extension involved in axon guidance decreased process quality, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
motor neuron axon increased branchiness, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 8
from Hosseinibarkooie et al., 2016
|
motor neuron decreased amount, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 5
from Sleigh et al., 2014
|
motor neuron axon bifurcated, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 5
from Sleigh et al., 2014
|
primary motor neuron axon length, ameliorated
|
ml2Tg + MO1-smn1
|
chemical treatment: terazosin
|
Fig. 6
from Boyd et al., 2017
|
primary motor neuron axon terminus swollen, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 6
from Boyd et al., 2017
|
fast muscle cell neuromuscular synaptic transmission decreased process quality, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
motor neuron axon branchiness, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 1
from Powis et al., 2016
|
motor neuron axon absent, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 5
from Sleigh et al., 2014
|
whole organism smn1 expression decreased amount, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
swimming behavior process quality, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 1
from Powis et al., 2016
|
fast muscle cell neuromuscular junction decreased width, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
primary motor neuron axonogenesis process efficacy, ameliorated
|
ml2Tg + MO1-smn1
|
chemical treatment: terazosin
|
Fig. 6
from Boyd et al., 2017
|
fast muscle cell neuromuscular junction development decreased process quality, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
CaP motoneuron collateral sprouting increased occurrence, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
motor neuron axon truncated, abnormal
|
ml2Tg + MO1-smn1
|
standard conditions
|
Fig. 8
from Hosseinibarkooie et al., 2016
Fig. 1
from Powis et al., 2016
Fig. 5
from Sleigh et al., 2014
|
motor neuron axon truncated, abnormal
|
ml2Tg + MO1-smn1 (EKW, TL)
|
standard conditions
|
Fig. 6
from Wishart et al., 2014
|
motor neuron axon branchiness, abnormal
|
ml2Tg + MO1-smn1 (EKW, TL)
|
standard conditions
|
Fig. 6
from Wishart et al., 2014
|
motor neuron axon increased branchiness, abnormal
|
ml2Tg + MO1-smn1 + MO2-smn1
|
standard conditions
|
Fig. 4
from Akten et al., 2011
|
motor neuron axon truncated, abnormal
|
ml2Tg + MO1-smn1 + MO2-smn1
|
standard conditions
|
Fig. 4
from Akten et al., 2011
|
motor neuron axon morphology, abnormal
|
ml2Tg + MO1-smn1 + MO2-smn1
|
standard conditions
|
Fig. 4
from Akten et al., 2011
|
motor neuron axon mislocalised, abnormal
|
os26Tg + MO1-smn1
|
standard conditions
|
Fig. 6
from Lotti et al., 2012
|
motor neuron axon truncated, abnormal
|
os26Tg + MO1-smn1
|
standard conditions
|
Fig. 1
from Lyon et al., 2014
|
motor neuron axon extension disrupted, abnormal
|
os26Tg + MO1-smn1
|
standard conditions
|
Fig. 2
from McGovern et al., 2015
|
motor neuron axon guidance decreased process quality, abnormal
|
os26Tg + MO1-smn1
|
standard conditions
|
Fig. 6
from Lotti et al., 2012
|
motor neuron axon morphology, abnormal
|
os26Tg + MO1-smn1
|
standard conditions
|
Fig. 2
from McGovern et al., 2015
Fig. 5
from Wiley et al., 2014
|
motor neuron axon branched, abnormal
|
os26Tg + MO1-smn1
|
standard conditions
|
Fig. 1
from Lyon et al., 2014
|
motor neuron axon truncated, abnormal
|
rw0Tg + MO1-smn1
|
standard conditions
|
Fig. 4
from McWhorter et al., 2003
|
motor neuron axon increased branchiness, abnormal
|
rw0Tg + MO1-smn1
|
standard conditions
|
Fig. 4
from McWhorter et al., 2003
|
motor neuron axon branchiness, abnormal
|
vu12Tg + MO1-smn1
|
standard conditions
|
Fig. 5
from Miller et al., 2015
|
motor neuron axon truncated, abnormal
|
vu12Tg + MO1-smn1
|
standard conditions
|
Fig. 5
from Miller et al., 2015
|
motor neuron axon increased branchiness, abnormal
|
vu12Tg + MO1-smn1
|
standard conditions
|
Fig. 2
from Edens et al., 2015
|
motor neuron axon decreased length, abnormal
|
vu12Tg + MO1-smn1
|
standard conditions
|
Fig. 2
from Edens et al., 2015
|
motor neuron axon extension process quality, abnormal
|
vu12Tg + MO1-smn1
|
standard conditions
|
Fig. 2
from Edens et al., 2015
|
motor neuron axon morphology, abnormal
|
vu12Tg + MO1-smn1
|
standard conditions
|
Fig. 5
from Miller et al., 2015
|
motor neuron axon truncated, abnormal
|
zf35Tg + MO1-smn1
|
standard conditions
|
Fig. 3
from McWhorter et al., 2003
|
motor neuron axon branched, abnormal
|
zf35Tg + MO1-smn1
|
standard conditions
|
Fig. 3
from McWhorter et al., 2003
|
neuron protein transport decreased rate, abnormal
|
ns12Tg/ns12Tg + MO1-smn1
|
standard conditions
|
FIGURE 3
from Koh et al., 2021
|
neuron regulation of protein oligomerization decreased rate, abnormal
|
ns12Tg/ns12Tg + MO1-smn1
|
standard conditions
|
FIGURE 3
from Koh et al., 2021
|
whole organism lethal (sensu genetics), abnormal
|
WT + MO1-pls3 + MO1-smn1
|
standard conditions
|
text only
from Oprea et al., 2008
|
whole organism ncaldb expression absent, abnormal
|
ml2Tg + MO1-ncaldb + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
CaP motoneuron axon length, ameliorated
|
ml2Tg + MO1-ncaldb + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
CaP motoneuron axon extension involved in axon guidance process quality, ameliorated
|
ml2Tg + MO1-ncaldb + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
fast muscle cell neuromuscular synaptic transmission process quality, ameliorated
|
ml2Tg + MO1-ncaldb + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
whole organism smn1 expression decreased amount, abnormal
|
ml2Tg + MO1-ncaldb + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
swimming rate, ameliorated
|
ml2Tg + MO1-ncaldb + MO1-smn1
|
standard conditions
|
Fig. S3
from Riessland et al., 2017
|
CaP motoneuron axon increased branchiness, abnormal
|
ml2Tg + MO1-ncaldb + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
fast muscle cell synaptic cleft width, ameliorated
|
ml2Tg + MO1-ncaldb + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
fast muscle cell neuromuscular junction width, ameliorated
|
ml2Tg + MO1-ncaldb + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
CaP motoneuron collateral sprouting increased occurrence, abnormal
|
ml2Tg + MO1-ncaldb + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|
fast muscle cell neuromuscular junction development process quality, ameliorated
|
ml2Tg + MO1-ncaldb + MO1-smn1
|
standard conditions
|
Fig. 3
from Riessland et al., 2017
|