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Allele Symbol Allele Name Allele ID |
Tg(Thy1-YFP)HJrs transgene insertion H, Joshua R Sanes MGI:3497947 |
| Summary |
19 genotypes |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• reduced number of dendritic intersections at a given distance from the soma of cortical layer 5 neuro
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• lack of inflammatory response in Japanese-encephalitis-infected neocortex
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at P28, mice have a greater percent of ON-OFF retinal ganglion cells (RGCs) than in control mice
• at P28, mice have fewer ON and OFF RGCs than controls
• at P28, mice have fewer numbers of ON RGC dendritic branches
• at P50, 55.4+/-4.3% of RGCs are bilaminated compared to 37.8+/-1.1% in controls
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• at P28, mice have fewer numbers of ON retinal ganglion cells (RGCs) dendritic branches
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• at P28, mice have a greater percent of ON-OFF retinal ganglion cells (RGCs) than in control mice
• at P28, mice have fewer ON and OFF RGCs than controls
• at P28, mice have fewer numbers of ON RGC dendritic branches
• at P50, 55.4+/-4.3% of RGCs are bilaminated compared to 37.8+/-1.1% in controls
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• dorsal CA1 neurons have smaller width of dendritic spine heads
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• dorsal CA1 neurons have smaller dendritic spines
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• dorsal CA1 neurons have fewer dendritic spines
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• dorsal CA1 neurons have shorter dendritic spines
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• dorsal CA1 neurons have reduced density and width of dendritic spines
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• dorsal CA1 neurons have reduced density of dendritic spines
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• retinal ganglion cell (RGC) axons sometimes exhibit defasciculation that forms a fork-like structures before reaching the optic nerve
• fascicles on RGC axons are smaller than in control mice
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• retinal ganglion cell axons sometimes exhibit defasciculation that forms a fork-like structures before reaching the optic nerve
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• retinal ganglion cell axons sometimes exhibit defasciculation that forms a fork-like structures before reaching the optic nerve
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• retinal ganglion cell (RGC) axons sometimes exhibit defasciculation that forms a fork-like structures before reaching the optic nerve
• fascicles on RGC axons are smaller than in control mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• the basal dendrites of layer V pyramidal neurons grow to the apical side with curling and collaterals from apical trunks show disorientation and winding
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• the basal dendrites of layer V pyramidal neurons grow to the apical side with curling and collaterals from apical trunks show disorientation and winding
• cortical neurons show an increase in the number of primary dendrites
• the highest number of dendrite crossings is found at about 40 um compared to 60-80 um in controls
• the basal dendritic field is further shifted to the apical part of the cell body and to the close part of cell body compared to mutant mice wild-type for Crmp1
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mice do not exhibit the neuron loss or increase in microglial density and migration velocity observed in Cx3cr1tm1Litt/Cx3cr1+ Psen1tm1Mpm/Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• microglial density increases over time around lost neurons unlike in Cx3cr1tm1Litt/Cx3cr1tm1Litt Psen1tm1Mpm/Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa mice
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• microglia migration velocity around lost neurons is 2-fold greater than in Cx3cr1tm1Litt heterozygotes and homozygotes
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• of YFP+ layer III neurons at 4 to 6 months
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• microglial density increases over time around lost neurons unlike in Cx3cr1tm1Litt/Cx3cr1tm1Litt Psen1tm1Mpm/Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa mice
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• microglia migration velocity around lost neurons is 2-fold greater than in Cx3cr1tm1Litt heterozygotes and homozygotes
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• microglial density increases over time around lost neurons unlike in Cx3cr1tm1Litt/Cx3cr1tm1Litt Psen1tm1Mpm/Psen1tm1Mpm Tg(APPSwe,tauP301L)1Lfa mice
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• microglia migration velocity around lost neurons is 2-fold greater than in Cx3cr1tm1Litt heterozygotes and homozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at mature stages all sensory axon exhibit a bifurcation failure compared to in wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at P3 with ectopic neurites extending towards the outer retina
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• at P3 with ectopic neurites extending towards the outer retina
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• cortical neurons show an increase in the number of primary dendrites
• the basal dendritic field is slightly shifted to the apical side of the cell body
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in vivo, dendritic spines of pyramidal neurons are less stable than spines on wild-type cells
• however, spine formation rate is normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in culture, dendrites of hippocampal at day 7 are 50% longer compared to wild-type neurons
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• dendritic trees of pyramidal cells in the CA1 region of the hippocampus are less complex than in wild-type mice
• the length of dendrites formed by granule cells in the dentate gyrus is increased (197+/-7 um compared to 164+/-7 um in wild-type mice)
• the complexity of apical dendrites in CA1 is reduced
• however, the complexity of granule cell dendrites in the dentate gyrus and the length of apical dendrites are normal
• in culture, dendrites of hippocampal neurons are 56% longer at day 3 and 88% longer at day 7 compared to wild-type neurons and the number of dendrites per cell is increased (1.8+/-0.2 compared to 1.2+/-0.1 for wild-type neurons) without affecting axon length, the number of axons per cell or the number of dendrites per cell
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mutants exhibit misorientation of apical dendrites in layer V pyramidal neurons in the visual cortex, but not in motor, somatosensory, or auditory cortices or in the upper layer of the visual cortex
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following treatment with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), seizures are more frequent and last longer than in similarly treated wild-type mice
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• mice treated with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) exhibit increased axonal damage, excitotoxicity, and behavioral deficits (including seizures, hindlimb and tail paresis, impaired coordination) compared with similarly treated wild-type mice
• however, activation of the N-methyl-D-aspartic acid (NMDA) receptors does not result in axonal injury
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• dorsal columns lack myelin unlike in wild-type mice
• mice exhibit amyelinated and hypomyelinated axons unlike in wild-type mice
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• mice exhibit amyelinated and hypomyelinated axons unlike in wild-type mice
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• following treatment with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA), seizures are more frequent and last longer than in similarly treated wild-type mice
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• on a rotarod at baseline and after treatment with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)
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• hindlimb and tail paresis following treatment with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)
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• mice treated with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) exhibit increased axonal damage, excitotoxicity, and behavioral deficits (including seizures, hindlimb and tail paresis, impaired coordination) compared with similarly treated wild-type mice
• however, activation of the N-methyl-D-aspartic acid (NMDA) receptors does not result in axonal injury
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• mice treated with alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) exhibit increased axonal damage, excitotoxicity, and behavioral deficits (including seizures, hindlimb and tail paresis, impaired coordination) compared with similarly treated wild-type mice
• however, activation of the N-methyl-D-aspartic acid (NMDA) receptors does not result in axonal injury
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• unlike in wild-type mice, the projections of dendrites and axons from pyramidal cells are disorganized
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• the number of pyramidal cells is decreased to 25% of that in wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• the ratio of corpus callosum:neocortex (CC:NCX) is disproportionately lower than that in wild-type controls
• the g-ratio (axon perimeter/axon+myelin perimeter) is significantly reduced, indicating decreased callosal axon thickness
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• L5 neocortical pyramidal neurons (PNs) exhibit significantly reduced soma size
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• EM analysis of transected corpus callosa revealed that the g-ratio (axon perimeter/axon+myelin perimeter) is significantly reduced, indicating smaller axon calibers
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• perforated patch recordings on neocortical pyramidal neurons revealed that the resting membrane potential is significantly more negative than that in wild-type neurons, consistent with lower intracellular ATP levels
• following treatment with tolbutamide (a K+ATP channel inhibitor), pyramidal neurons fail to exhibit a more positive membrane potential, unlike in wild-type neurons
• following treatment with sodium azide (NaN3), a complex IV inhibitor that indirectly decreases ATP, pyramidal neurons fail to exhibit a significant decrease in membrane potential, unlike in wild-type neurons
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• EM analysis of L5 neocortical pyramidal neurons revealed an increase in mitochondrial density and a more rounded shape, consistent with increased mitochondrial fission
• however, cumulative mitochondrial coverage, area, and perimeter remain normal
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• L5 neocortical pyramidal neurons exhibit a more rounded mitochondrial shape (decreased aspect ratio)
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• L5 neocortical pyramidal neurons exhibit an increase in mitochondrial density
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• isolated neocortical mitochondria exhibit reduced ATP production in a luciferase-based ATP synthesis assay
• however, mitochondrial membrane potential and reactive oxygen species (ROS) production are normal
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• L5 neocortical pyramidal neurons exhibit dysmorphic mitochondria typical of increased mitochondrial fission
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• cultured primary neocortical neurons show a significant reduction in basal oxygen consumption rate (OCR) relative to wild-type neurons
• following FCCP treatment to maximize mitochondrial respiration, primary neocortical neurons cannot respire at as high of a rate as wild-type neurons
• however, no differences in OCR are observed in response to oligomycin or antimycinA/rotenone treatment (OXPHOS-inhibiting drugs)
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 04/23/2024 MGI 6.23 |
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