All Phenotypes Tg(tetO-SNCA*A53T)E2Cai MGI Mouse

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Phenotypes associated with this allele

Allele Symbol
Allele Name
Allele ID

Tg(tetO-SNCA*A53T)E2Cai
transgene insertion E2, Huaibin Cai
MGI:4420801

Summary

11 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cx1	Pitx3^tm1.1Cai/Pitx3⁺ Tg(tetO-SNCA*A53T)E2Cai/0	involves: 129 * C57BL/6J * FVB/N	MGI:5432013
cx2	Pink1^tm1Zhzh/Pink1^tm1Zhzh Slc6a3^tm4.1(tTA)Xz/? Tg(tetO-SNCA*A53T)E2Cai/?	involves: 129P2/OlaHsd * 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6	MGI:5619815
cx3	Slc6a3^tm4.1(tTA)Xz/Slc6a3⁺ Tg(tetO-SNCA*A53T)E2Cai/0	involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6	MGI:5619812
cx4	Prkn^tm1Shn/Prkn^tm1Shn Slc6a3^tm4.1(tTA)Xz/? Tg(tetO-SNCA*A53T)E2Cai/?	involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6	MGI:5619814
cx5	Lrrk2^tm1.1Cai/Lrrk2⁺ Tg(Camk2a-tTA)1Mmay/0 Tg(tetO-SNCA*A53T)E2Cai/0	involves: 129X1/SvJ * C57BL/6	MGI:4421006
cx6	Lrrk2^tm1.1Cai/Lrrk2^tm1.1Cai Tg(Camk2a-tTA)1Mmay/0 Tg(tetO-SNCA*A53T)E2Cai/0	involves: 129X1/SvJ * C57BL/6	MGI:4421016
cx7	Tg(Camk2a-tTA)1Mmay/0 Tg(tetO-LRRK2)C77Cai/0 Tg(tetO-SNCA*A53T)E2Cai/0	involves: C57BL/6	MGI:4420996
cx8	Tg(Camk2a-tTA)1Mmay/0 Tg(tetO-LRRK2)D10Cai/0 Tg(tetO-SNCAA53T)E2Cai/0	involves: C57BL/6	MGI:4420998
cx9	Tg(Camk2a-tTA)1Mmay/0 Tg(tetO-LRRK2G2019S)E3Cai/0 Tg(tetO-SNCAA53T)E2Cai/0	involves: C57BL/6	MGI:4421000
cx10	Tg(Camk2a-tTA)1Mmay/0 Tg(tetO-LRRK2)C7874Cai/0 Tg(tetO-SNCA*A53T)E2Cai/0	involves: C57BL/6	MGI:4421002
cx11	Tg(Camk2a-tTA)1Mmay/0 Tg(tetO-SNCA*A53T)E2Cai/0	involves: C57BL/6	MGI:4421003

Allelic Composition	Pitx3^tm1.1Cai/Pitx3⁺ Tg(tetO-SNCA*A53T)E2Cai/0
Genetic Background	involves: 129 * C57BL/6J * FVB/N

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pitx3^tm1.1Cai mutation (1 available); any Pitx3 mutation (22 available)
Tg(tetO-SNCA*A53T)E2Cai mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

microgliosis ( J:185958 )

• at 20 months

astrocytosis ( J:185958 )

• at 20 months

abnormal dopaminergic neuron morphology ( J:185958 )

• at 1 month, midbrain dopamine (mDA) neurons exhibit enlarged axon terminals compared with control cells

• at 12 months, mDA neurons exhibit perturbations of the Golgi apparatus compared with control mice

loss of dopaminergic neurons ( J:185958 )

• progressive degeneration of midbrain dopamine neurons as early as 1 month

• however, there is no loss of midbrain dopamine neurons between 12 and 20 months and inhibition of Nurr1 (Nr4a2) ameliorates loss of neurons

abnormal neurite morphology ( J:185958 )

• at 12 months, neurites exhibit reduced length and complexity compared with control neurites

neuron degeneration ( J:185958 )

• progressive degeneration of midbrain dopamine neurons as early as 1 month

• however, there is no loss of midbrain dopamine neurons between 12 and 20 months

alpha-synuclein inclusion body ( J:185958 )

• in the soma and neurites of midbrain dopamine neurons at 12 and 18 months

abnormal neuron physiology ( J:185958 )

• midbrain dopamine neurons exhibit impaired

• autophagy/lysosomal pathways and ubiquitin proteasome system pathway compared with control cells

abnormal synaptic dopamine release ( J:185958 )

• severely impaired in the striatum

behavior/neurological

impaired coordination ( J:185958 )

• on a rotarod at 2 months

abnormal gait ( J:185958 )

• unsteady and shorter at 1 month

short stride length ( J:185958 )

• at 1 month

decreased vertical activity ( J:185958 )

• at 1 months

• however, mice fed doxycycline treatment rescues rearing impairment

decreased locomotor activity ( J:185958 )

• moderate starting at 2 months in an open field

cellular

abnormal autophagy ( J:185958 )

• impaired autophagy/lysosome pathways in midbrain dopamine neurons

growth/size/body

slow postnatal weight gain ( J:185958 )

• at 2 months

hematopoietic system

microgliosis ( J:185958 )

• at 20 months

homeostasis/metabolism

abnormal autophagy ( J:185958 )

• impaired autophagy/lysosome pathways in midbrain dopamine neurons

decreased dopamine level ( J:185958 )

• at 6 months in the striatum

immune system

microgliosis ( J:185958 )

• at 20 months

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Parkinson's disease		DOID:14330	OMIM:PS168600	J:185958

Allelic Composition	Pink1^tm1Zhzh/Pink1^tm1Zhzh Slc6a3^tm4.1(tTA)Xz/? Tg(tetO-SNCA*A53T)E2Cai/?
Genetic Background	involves: 129P2/OlaHsd * 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pink1^tm1Zhzh mutation (0 available); any Pink1 mutation (43 available)
Slc6a3^tm4.1(tTA)Xz mutation (1 available); any Slc6a3 mutation (66 available)
Tg(tetO-SNCA*A53T)E2Cai mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

cellular

abnormal mitochondrial morphology ( J:218892 )

• 51% reduction of mitochondrial mass at 3 weeks of age

nervous system

neuronal cytoplasmic inclusions ( J:218892 )

• "mitochondrial inclusions are observed in in dopaminergic neurons beginning at 3 weeks of age

• inclusions average 4.2 um in diameter and are labeled by mitochondrial markers (COX1, SOD2)

• number of inclusions is approximately 1.4 inclusions per dopaminergic neuron

Allelic Composition	Slc6a3^tm4.1(tTA)Xz/Slc6a3⁺ Tg(tetO-SNCA*A53T)E2Cai/0
Genetic Background	involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Slc6a3^tm4.1(tTA)Xz mutation (1 available); any Slc6a3 mutation (66 available)
Tg(tetO-SNCA*A53T)E2Cai mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

loss of dopaminergic neurons ( J:218892 )

• 21% dopaminergic neuron loss in the substantia nigra pars compacta (SNc) by 3 months of age

• 35% loss by 6 months of age

• loss appears to stop or slow between 6 and 12 months

• dopamine turnover rate is increased by 29%

• decrease in TH (tyrosine hydroxylase) terminal staining in the dorsal, but not ventral, striatum of 12 month old mice

abnormal axon morphology ( J:218892 )

• 25 fold increase in enlarged axon varicosities in midbrain region at 6 weeks of age

• varicosities are approximately 10 um in diameter, are oval-shaped and have a hollowed core

abnormal dendrite morphology ( J:218892 )

• fragmented dendrites are observed in the substantia nigra pars reticulata at 6 weeks of age

neuron degeneration ( J:218892 )

neuronal cytoplasmic inclusions ( J:218892 )

• "mitochondrial inclusions" are observed in dopaminergic neurons beginning at 3 weeks of age

• inclusions are 0.5-2 um in diameter and are labeled by mitochondrial markers (COX1, SOD2)

• number of inclusions is approximately 1.6 inclusions per dopaminergic neuron at 3 weeks of age

• inclusions are distributed in soma and proximal processes of dopaminergic neurons

• inclusions are mostly restricted to substantia nigra pars compacta

• the number of inclusions is decreased by 6 months of age

growth/size/body

slow postnatal weight gain ( J:218892 )

homeostasis/metabolism

decreased dopamine level ( J:218892 )

• levels of dopamine and its metabolites (DOPA and HVA) are decreased by 54% in 7-11 month old mice in striatal tissue

cellular

abnormal mitochondrial shape ( J:218892 )

• mitochondria in dopaminergic neurons appears fragmented by 6 weeks of age

decreased mitochondrial size ( J:218892 )

• mitochondrial length is decreased by 61% in mitochondria from dopaminergic neurons, however, mitochondrial mass is similar to controls

abnormal mitochondrial physiology ( J:218892 )

• multiple senescent mitochondria are observed in dopaminergic neurons as compared to controls

• senescent mitochondria exhibit disordered cristae, swollen matrix and the absent outer membranes

Allelic Composition	Prkn^tm1Shn/Prkn^tm1Shn Slc6a3^tm4.1(tTA)Xz/? Tg(tetO-SNCA*A53T)E2Cai/?
Genetic Background	involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Prkn^tm1Shn mutation (3 available); any Prkn mutation (54 available)
Slc6a3^tm4.1(tTA)Xz mutation (1 available); any Slc6a3 mutation (66 available)
Tg(tetO-SNCA*A53T)E2Cai mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

neuronal cytoplasmic inclusions ( J:218892 )

• "mitochondrial inclusions are observed in in dopaminergic neurons beginning at 3 weeks of age

• inclusions average 4.4 um in diameter and are labeled by mitochondrial markers (COX1, SOD2)

• number of inclusions is approximately 1.7 inclusions per dopaminergic neuron

cellular

abnormal mitochondrial morphology ( J:218892 )

• 57% reduction of mitochondrial mass at 3 weeks of age

Allelic Composition	Lrrk2^tm1.1Cai/Lrrk2⁺ Tg(Camk2a-tTA)1Mmay/0 Tg(tetO-SNCA*A53T)E2Cai/0
Genetic Background	involves: 129X1/SvJ * C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Lrrk2^tm1.1Cai mutation (1 available); any Lrrk2 mutation (159 available)
Tg(Camk2a-tTA)1Mmay mutation (8 available)
Tg(tetO-SNCA*A53T)E2Cai mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal nervous system morphology ( J:156512 )

• somatic alpha synuclein in neurons is apparent at 12 months

microgliosis ( J:156512 )

• increased microglial activation is observed in the brain at 12 months

abnormal striatum morphology ( J:156512 )

• numbers of residual neurons is significantly lower than non transgenic controls

astrocytosis ( J:156512 )

• significant at 12 months

abnormal neuron morphology ( J:156512 )

• the Golgi complex shows severe fragmentation in 12 month old animals

neurodegeneration ( J:156512 )

• neurodegeneration significant at 12 months

immune system

microgliosis ( J:156512 )

• increased microglial activation is observed in the brain at 12 months

hematopoietic system

microgliosis ( J:156512 )

• increased microglial activation is observed in the brain at 12 months

Allelic Composition	Lrrk2^tm1.1Cai/Lrrk2^tm1.1Cai Tg(Camk2a-tTA)1Mmay/0 Tg(tetO-SNCA*A53T)E2Cai/0
Genetic Background	involves: 129X1/SvJ * C57BL/6

Find Mice

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

nervous system phenotype ( J:156512 )

N	• no apparent neurodegeneration is observed in 12-month old mice; no significant elevation of astrocytosis, microgliosis or somatic accumulation of alpha-synuclein is detected in striatum at 12 months

Allelic Composition	Tg(Camk2a-tTA)1Mmay/0 Tg(tetO-LRRK2)C77Cai/0 Tg(tetO-SNCA*A53T)E2Cai/0
Genetic Background	involves: C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Camk2a-tTA)1Mmay mutation (8 available)
Tg(tetO-LRRK2)C77Cai mutation (0 available)
Tg(tetO-SNCA*A53T)E2Cai mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal nervous system morphology ( J:156512 )

• increasing accumulation of alpha-synuclein is detected in cell bodies in brains of A53T/LRRK2WT-L at 1 month compared to LRRK2WT-L animals

microgliosis ( J:156512 )

• increased microglial activation is observed in the brain

astrocytosis ( J:156512 )

• A53T/LRRK2WT-L mice show significant elevation of GFAP-positive astrocytes in the striatum compared to A53T mice

neurodegeneration ( J:156512 )

• neurodegeneration is accelerated in the striatum

abnormal nervous system physiology ( J:156512 )

• increasing accumulation of alpha-synuclein is detected in cell bodies at 1 month

behavior/neurological

abnormal locomotor behavior ( J:156512 )

• mice show no apparent motor phenotype up to 6 months of age

hematopoietic system

microgliosis ( J:156512 )

• increased microglial activation is observed in the brain

immune system

microgliosis ( J:156512 )

• increased microglial activation is observed in the brain

Allelic Composition	Tg(Camk2a-tTA)1Mmay/0 Tg(tetO-LRRK2)D10Cai/0 Tg(tetO-SNCAA53T)E2Cai/0
Genetic Background	involves: C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Camk2a-tTA)1Mmay mutation (8 available)
Tg(tetO-LRRK2*)D10Cai mutation (0 available)
Tg(tetO-SNCA*A53T)E2Cai mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal nervous system morphology ( J:156512 )

• increasing accumulation of alpha-synuclein is detected in cell bodies at 1 month in A53T/KD mice compared to KD animals

abnormal neuron morphology ( J:156512 )

• increased framentation of the Golgi complex is observed

abnormal nervous system physiology ( J:156512 )

• neuropathology is accelerated in A53T/KD mice compared to A53T mice

Allelic Composition	Tg(Camk2a-tTA)1Mmay/0 Tg(tetO-LRRK2G2019S)E3Cai/0 Tg(tetO-SNCAA53T)E2Cai/0
Genetic Background	involves: C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Camk2a-tTA)1Mmay mutation (8 available)
Tg(tetO-LRRK2*G2019S)E3Cai mutation (1 available)
Tg(tetO-SNCA*A53T)E2Cai mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal nervous system morphology ( J:156512 )

• substantial accumulation of alpha-synuclein is detected in cell bodies at 1 month

microgliosis ( J:156512 )

• exacerbated in the striatum compared to A53T mice at 1 month of age

• levels of microglial activation are higher than in A53T/LRRK2WT mice

abnormal dorsal striatum morphology ( J:156512 )

astrocytosis ( J:156512 )

• exacerbated in the striatum compared to A53T mice at 1 month of age

• levels of GFAP-positive cells are higher than in A53T/LRRK2WT mice

abnormal neuron morphology ( J:156512 )

• the Golgi complex is drastically altered in neurons at 1 month with severely fragmented

• at 1 month, the medial/trans-Golgi in neurons is severely fragmented

abnormal neuron mitochondrial morphology ( J:156512 )

• in striatal neurons at 1 month, numerous mitochondria have denser matrices and widened cristae compared to controls or A53T mice (seen with 3.5x greater frequency than in A53T mice); these mitochondria are not functional

alpha-synuclein inclusion body ( J:156512 )

• a significant increase in detergent-insoluble high molecular weight (HMW) alpha synuclein is detected in 1 month old mice compared to A53T age-matched mice

neurodegeneration ( J:156512 )

• exacerbated in the striatum compared to A53T mice at 1 month of age

• dramatic loss (>85%) of striatal neurons is seen in the dorsal striatum

hematopoietic system

microgliosis ( J:156512 )

• exacerbated in the striatum compared to A53T mice at 1 month of age

• levels of microglial activation are higher than in A53T/LRRK2WT mice

immune system

microgliosis ( J:156512 )

• exacerbated in the striatum compared to A53T mice at 1 month of age

• levels of microglial activation are higher than in A53T/LRRK2WT mice

cellular

abnormal neuron mitochondrial morphology ( J:156512 )

Allelic Composition	Tg(Camk2a-tTA)1Mmay/0 Tg(tetO-LRRK2)C7874Cai/0 Tg(tetO-SNCA*A53T)E2Cai/0
Genetic Background	involves: C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Camk2a-tTA)1Mmay mutation (8 available)
Tg(tetO-LRRK2)C7874Cai mutation (2 available)
Tg(tetO-SNCA*A53T)E2Cai mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

nervous system

abnormal nervous system morphology ( J:156512 )

• increasing accumulation of alpha-synuclein is detected in cell bodies at 1 month compared to A53T/LRRK2WT-L animals

microgliosis ( J:156512 )

• increased microglial activation is observed in the brain

abnormal dorsal striatum morphology ( J:156512 )

• neuron loss is detected at 6 months and later

abnormal cerebral cortex morphology ( J:156512 )

astrocytosis ( J:156512 )

• A53T/LRRK2WT mice show significant elevation of GFAP-positive astrocytes in the striatum compared to A53T mice

• more GFAP-positive astrocytes are found in the brain than in A53T/LRRK2WT-L brains

abnormal neuron morphology ( J:156512 )

• the Golgi complex is drastically altered in neurons at 1 month with severely fragmented cis-Golgi

• at 1 month, the medial/trans-Golgi in neurons is severely fragmented

neurodegeneration ( J:156512 )

• neurodegeneration is accelerated in the striatum

• dramatic loss (>80%) of striatal neurons is seen in the dorsal striatum

• most degenerating neurons are striatal medium-sized spiny neurons (MSN)

abnormal nervous system physiology ( J:156512 )

• neuropathology is accelerated in mice compared to A53T mice

• in 6 month old mice, elevated levels of ubiquitin are detected in somas and nuclei of cortical neurons; levels of alpha-synuclein and ubiquitin are slightly higher than in A53T mutant mice

• brain homogenates contain significantly elevated levels of ubiquitinated proteins at 3 months

immune system

microgliosis ( J:156512 )

• increased microglial activation is observed in the brain

hematopoietic system

microgliosis ( J:156512 )

• increased microglial activation is observed in the brain

Allelic Composition	Tg(Camk2a-tTA)1Mmay/0 Tg(tetO-SNCA*A53T)E2Cai/0
Genetic Background	involves: C57BL/6

Find Mice

Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Camk2a-tTA)1Mmay mutation (8 available)
Tg(tetO-SNCA*A53T)E2Cai mutation (1 available)

♀	phenotype observed in females
♂	phenotype observed in males
N	normal phenotype

growth/size/body

decreased body weight ( J:156512 )

• A53T mice weigh significantly less than non transgenic mice and Tg(tetO-SNCA*A53T)E2Cai or Tg(Camk2a-tTA)1Mmay single mutants starting at 4 months of age

behavior/neurological

abnormal locomotor activation ( J:156512 )

increased vertical activity ( J:156512 )

• mice display elevated rearing activities at 6 months of age

increased locomotor activity ( J:156512 )

• at 2 months of age, mice show drastically increased ambulatory activity

nervous system

abnormal nervous system morphology ( J:156512 )

• only a few neurons in the brain display alpha-synuclein staining in the cell body at 3 months; somatic accumulation becomes more prominent at 20 months; whereas no accumulation is detected in cell bodies at 1 month

• significant rescue of phenotype is observed when animals are treated with doxycycline to inhibit transgene expression

microgliosis ( J:156512 )

• significant at 12 months

• significant rescue of phenotype is observed when animals are treated with doxycycline to inhibit transgene expression

abnormal striatum morphology ( J:156512 )

• neuron loss is detected at 6 months and later

• significant rescue of phenotype is observed when animals are treated with doxycycline to inhibit transgene expression

abnormal cerebral cortex morphology ( J:156512 )

• neuron loss is detected at 6 months and later

• in 6 month old mice but not in nontransgenic controls, elevated levels of ubiquitin are detected in somas and nuclei of cortical neurons, but

astrocytosis ( J:156512 )

• significant at 12 months

• significant rescue of phenotype is observed when animals are treated with doxycycline to inhibit transgene expression

abnormal neuron morphology ( J:156512 )

• the Golgi complex is drastically altered in neurons at 1 month, appearing thinner and fragmented

• significant increase in Golgi fragmentation is observed at 6 months

• at 1 month, the medial/trans-Golgi in neurons is significantly altered with ratio of fragmented trans-Golgi significantly increased compared to non-transgenic animals

• significant rescue of phenotype is observed when animals are treated with doxycycline to inhibit transgene expression

abnormal neuron mitochondrial morphology ( J:156512 )

• in striatal neurons at 1 month, numerous mitochondria have denser matrices and widened cristae compared to non-transgenic controls; these mitochondria are not functional

alpha-synuclein inclusion body ( J:156512 )

• a significant increase in detergent-insoluble high molecular weight (HMW) alpha synuclein is detected in 12 month old mice compared to 1 month old mice

• significant decrease in HMW alpha-synuclein in total brain homogenates is observed when animals are treated with doxycycline to inhibit transgene expression

neurodegeneration ( J:156512 )

• widespread degeneration is observed at 20 months

• age-dependent, progressive neurodegeneration occurs

• neuronal loss is detected in the frontal cortex (>80%) and dorsal striatum (>74%) at 20 months

• a significant reduction (>30%) of striatal neurons is seen at 6 months

abnormal nervous system physiology ( J:156512 )

• while 3-month old A53T mice show no abnormal neuropathology, but neuropathology is evident at 12 and 20 months

• in 6 month old mice, elevated levels of ubiquitin are detected in somas and nuclei of cortical neurons; at 20 monts, a punctate staining pattern at neuronal processes is observed

• brain homogenates contain significantly elevated levels of ubiquitinated proteins at 3 months

hematopoietic system

microgliosis ( J:156512 )

• significant at 12 months

• significant rescue of phenotype is observed when animals are treated with doxycycline to inhibit transgene expression

immune system

microgliosis ( J:156512 )

• significant at 12 months

• significant rescue of phenotype is observed when animals are treated with doxycycline to inhibit transgene expression

cellular

abnormal neuron mitochondrial morphology ( J:156512 )

• in striatal neurons at 1 month, numerous mitochondria have denser matrices and widened cristae compared to non-transgenic controls; these mitochondria are not functional

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