Overview

The PS19 mouse model harbors the T34 isoform of microtubule-associated protein tau with one N-terminal insert and four microtubule binding repeats (1N4R) encoding the human P301S mutation, all driven by the mouse prion protein promoter. These mice are useful in studying neurofibrillary tangles, neurodegenerative tauopathy and Alzheimer's disease.

Donating Investigator

Virginia M Lee, University of Pennsylvania

Genetic overview

Genetic Background	Generation
	?+N3F8 (2018-01-16 00:00:00)

Tg(Prnp-MAPT*P301S)PS19Vle

Allele Type
Transgenic (Inserted expressed sequence, Humanized sequence)

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Research Applications

Neurobiology Research

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Base Price

Starting at:

$263.00 Domestic price for female 4-week

339.22 Domestic price for breeder pair

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Details

Detailed Description

These PS19 transgenic mice (P301S Tg mice) express the P301S mutant form of human microtubule-associated protein tau (MAPT), under the direction of the mouse prion protein promoter (Prnp).

The expression of the mutant human MAPT is five-fold higher than the expression of the endogenous mouse MAPT protein. Hyperphosphorylated, insoluble mutant human MAPT protein in the brain accumulates with age causing decreased microtubule binding/density. At three months of age, transgenic mice exhibit clasping and limb retraction when lifted by the tail, which progresses to limb weakness. By ten months of age the mice exhibit a hunched back and paralysis, followed by inability to feed. Transgenic mice have a median lifespan of approximately nine months with approximately 80% dying by 12 months. Histological analysis reveals neuron degeneration in hippocampus and ventricular dilatation (brain atrophy) by eight months of age, although significant neuron degeneration in the hippocampus occurs at approximately nine months of age. Neuron loss spreads to the amygdala, neocortex and entorhinal cortex by 12 months of age. Defective translocation of endoplasmic reticulum proteins in affected neurons is observed as early as three months of age. The onset of neurofibrillay tangle formation in the neocortex, amygdala, hippocampus, brain stem and spinal cord is five months of age. Transgenic mice display neuroinflammation with microglial activation and astrogliosis. The ultrastructure of the neurofibrillay tangle-like lesions detected is similar to that found in brain lesions of human Alzheimer's disease and tauopathy patients. Degradation of synaptic function is significant by six months of age. These mice cannot be bred to homozygosity as homozygous females do not mate.

The phenotype of PS19 transgenic mice described above is based on the published information available as of 2008. In 2012-2013, publications using PS19 mice on a B6C3F1 or B6C3 genetic background report attenuated formation of tau pathology (hyperphosphorylated tau inclusions prominent by 12 months of age, significant neuronal death after 12 months of age), as well as males developing tau pathology more consistently than females. It is not determined if these phenotype differences are observed for the PS19 colony at The Jackson Laboratory. To ensure genetically stability, we periodically refresh our colony onto the hybrid B6C3F1/J genetic background (Stock No. 100010). This was last performed March to November 2016.

As of October 2017, the Stock No. 008169 live colony is homozygous for the C57BL/6-derived functional Pde6b⁺ allele (the C3H-derived Pde6b^rd1 allele has been selectively removed). Additionally, this B6;C3H background strain has not been monitored/selected for other inbred background-specific loci (e.g., Tlr4⁺ vs. Tlr4^Lps-d).

Development

The P301S transgene was designed with the P301S mutant human microtubule-associated protein tau (MAPT*P301S) under the direction of the mouse prion protein promoter (Prnp). This transgene was injected into fertilized B6C3F1 mouse eggs. Transgenic founder animals were bred to B6C3F1/J or B6C3F1/Crl mice to establish founder line 19 (PS19). The resulting PS19 colony was maintained as hemizygotes on the B6C3F1 background before sending to The Jackson Laboratory Repository in 2008.

As of October 2017, the Stock No. 008169 live colony is homozygous for the C57BL/6-derived functional Pde6b⁺ allele (the C3H-derived Pde6b^rd1 allele has been selectively removed). Additionally, this B6;C3H background strain has not been monitored/selected for other inbred background-specific loci (e.g., Tlr4⁺ vs. Tlr4^Lps-d).

Expression Data

Expressed Gene	MAPT, microtubule associated protein tau, human
Site of Expression

Control Suggestions

Noncarrier

Approximate Controls

100010 B6C3F1/J

Additional Information

Considerations for Choosing Controls

Selected References

Yoshiyama Y; Higuchi M; Zhang B; Huang SM; Iwata N; Saido TC; Maeda J; Suhara T; Trojanowski JQ; Lee VM. 2007. Synapse loss and microglial activation precede tangles in a P301S tauopathy mouse model. Neuron 53(3):337-51PubMed: 17270732 MGI: J:119741

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Genetics

Tg(Prnp-MAPT*P301S)PS19Vle

Allele Symbol: Tg(Prnp-MAPT*P301S)PS19Vle

Allele Name	transgene insertion PS19, Virginia M Y Lee
Allele Type	Transgenic (Inserted expressed sequence, Humanized sequence)
Allele Synonym(s)	Tg(Prnp-MAPT*P301S)PS19Vle; transgene insertion PS19, Virginia M Y Lee
Gene Symbol and Name	Tg(Prnp-MAPT*P301S)PS19Vle, transgene insertion PS19, Virginia M Y Lee
Gene Synonym(s)	P301S tau (line PS19); PS19 Tg
Promoter	Prnp, prion protein, mouse, laboratory
Expressed Gene	MAPT, microtubule associated protein tau, human
Strain of Origin	(C57BL/6 x C3H)F1
Chromosome	3
Molecular Note	The transgene construct contains the P301S mutant human microtubule-associated protein tau, MAPT, under the direction of the mouse prion protein, Prnp, promoter. The expression of the mutant human MAPT is 5-fold higher than the expression of the endogenous mouse Mapt protein. Transgene insertion occurred on Chr 3, causing a 249 Kb deletion.
Mutations Made By	Virginia Lee, University of Pennsylvania

Disease/Phenotype

Disease Terms

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Alzheimer's disease

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Neurobiology Research
- Alzheimer's Disease
- Neurodegeneration

Genotype: Tg(Prnp-MAPT*P301S)PS19Vle related

Neurobiology Research
- Alzheimer's Disease
  - Tau (Mapt) mutants

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Tg(Prnp-MAPTP301S)PS19Vle/0
B6.Cg-Tg(Prnp-MAPTP301S)PS19Vle

behavior/neurological phenotype

abnormal behavior
- in the Barnes circular maze test, males are able to locate the correct target hole where the escape box had been in the probe trial, however they spend less time around the target hole than wild-type mice
- in the Y-maze test, the total percentage of alternations is decreased indicating impaired spontaneous alternation

abnormal contextual conditioning behavior
- in the contextual fear conditioning test, mutants show decreased immobility in the fourth time point only

abnormal emotion/affect behavior
- in a portion of the Porsolt forced swim test, mutants show decreased immobility time and increased distance traveled, suggesting that despair-like behavior might be decreased, however, generally over the entire test, no statistical significance is seen for immobility
- r immobility

abnormal social investigation
- Normal - however, no differences were seen in the social interaction test of a one-chamber novel environment
- in Crawley's three-chamber social approach test, males spend a shorter time with stranger mice than with familiar mice compared to wild-type mice which spend more time with stranger mice, indicating some impaired sociability or object recognition memory

decreased anxiety-related response
- in the elevated plus-maze test, entries into and time spent on the open arms is increased and in the open field test, time spent in the center of the field is increased, indicating decreased anxiety-like behavior

decreased thermal nociceptive threshold
- males exhibit decreased thresholds in the hot plate test, indicating increased antinociceptive responses

hyperactivity
- in the open field test, 14 week old males show an increase in total locomotive distance and an increase in stereotypic locomotion
- in the Y-maze test, males show increased numbers of entries into each arm, total alternations, and total distance traveled indicating hyperactivity

increased vertical activity
- vertical activity of 14 week old males is increased in the latter half of the open field test

integument phenotype

decreased thermal nociceptive threshold
- males exhibit decreased thresholds in the hot plate test, indicating increased antinociceptive responses

nervous system phenotype

increased prepulse inhibition
- males younger than 6 months of age exhibit lower startle amplitudes than wild-type mice at 110 dB and 120 dB and an increase in percent prepulse inhibition

tau protein deposits
- hyperphosphorylated tau protein accumulation is seen in the lateral globus pallidus, amygdala, auditory cortex, ventral hippocampus, the cingulate cortex, anterior cortical amygdaloid nucleus, and dorsal hippocampus at 4 months of age

The following phenotype relates to a compound genotype created using this strain

Genotype: Tg(Prnp-MAPTP301S)PS19Vle/Tg(Prnp-MAPTP301S)PS19Vle
involves: C3H * C57BL/6

behavior/neurological phenotype

abnormal sexual interaction
- homozygous females do not mate, so mice have to be maintained as hemizygotes

Genotype: Tg(Prnp-MAPTP301S)PS19Vle/0
involves: C3H C57BL/6

behavior/neurological phenotype

abnormal spatial learning
- 6 month old females are able to learn to locate the platform of the Morris water maze during training and latencies to find the visible platform are similar between mutants and wild-type mice, however mutants spend more time in finding the invisible platform, indicating impaired spatial learning ability
- during the probe trail of the Morris water maze, mutant females show less time and path length in the pool quadrant where the platform had previously been placed and a smaller number of target platform crossings
- orm, indicating impaired spatial learning ability

hunched posture
- paralysis is associated with hunched-back posture

limb grasping
- at 3 months of age, mice exhibit limb grasping and limb retraction when lifted by the tail, whereas mice expressing a wild-type MAPT transgene show no neurodegenerative phenotype up to 24 months of age

paralysis
- 44% of mutants exhibit paresis or paralysis and presence of a hunchback posture at 11 months of age
- mice show paralysis at 7-10 months of age

paresis
- 44% of mutants exhibit paresis or paralysis and presence of a hunchback posture at 11 months of age

weakness
- limb grasping at 3 months of age is followed by limb weakness

growth/size/body region phenotype

weight loss
- slight decrease in weight is seen at 11 months of age

mortality/aging

premature death
- ~80% of mice die by 12 months of age, with median survival of ~9 months

muscle phenotype

dystrophic muscle
- affected muscles show group atrophies with small angular fibers, indicating chronic denervation of motor neurons

progressive muscle weakness
- mice show motor increasing weakness and neurogenic muscular atrophy after 3 months of age

nervous system phenotype

abnormal amygdala morphology
- neuron loss is observed at 12 months of age

abnormal cerebral cortex morphology
- at 3 months, mice have neurofilament light chain and tau-positive spheroids in the cerebral cortex
- prominent atrophy of neocortex is observed at 9 months of age, with a 20% reduction in volume at 12 months of age

abnormal CNS synaptic transmission
- basal synaptic transmission is impaired at 6 months
- mice show small fiber volley amplitude, fEPSP slopes and amplitudes at all stimulus intensities tested

abnormal dentate gyrus morphology
- at 3 months, mice have neurofilament light chain and tau-positive spheroids in the dentate gyrus, as well as in the cortex

abnormal entorhinal cortex morphology
- neuron loss is observed at 12 months of age

abnormal excitatory postsynaptic potential
- at 6 months, the maximum fEPSP is reduced relative to wild-type MAPT transgenic mice

abnormal hippocampal mossy fiber morphology
- at 3 months but not at 6 months, neurofilament light chain-positive mossy fibers are not detected in CA3 of hippocampus
- at 3 months but not at 6 months, neurofilament light chain-positive mossy fibers are not detected in CA3 of hippocampus at 3 months but not at 6 months, neurofilament light chain-positive mossy fibers are not detected in CA3 of hippocampus

abnormal hippocampus pyramidal cell morphology
- significant reduction in number in the hippocampal CA3 region is found at 12 months of age, but no loss is detected at 6 months

abnormal spinal cord white matter morphology
- at 3 months, mice have neurofilament light chain and tau-positive spheroids in the spinal cord white matter

astrocytosis
- gliosis is striking at 6 months in the white matter where little tau pathology exists
- microglial activation precedes astrogliosis in brain regions containing NFTs; this is found in the brain and spinal cord, especially in white matter at 3 months of age with increases seen at 6 months in white and gray matter of hippocampus, amygdala, entorhinal cortex and spinal cord
- rhinal cortex and spinal cord
- younger mice (3-4 months) show no overt gliosis but increased microglial activation is detected in the hippocampus

brain atrophy
- limb grasping at 3 months of age is followed by brain atrophy

decreased hippocampus volume
- ~25% and ~40% reductions in hippocampal volume at 9 and 12 months of age respectively

decreased paired-pulse facilitation
- at 6 months, mice show significantly reduce paired pulse facilitation (PPF) ratio at all stimulus intervals

dilated brain ventricles
- by 8 months of age, ventricular dilatation is seen

hippocampal neuron degeneration

hippocampus atrophy
- marked hippocampal atrophy at 9 months of age

loss of hippocampal neurons
- up to 6 months, mice show no neuron loss, but by 8 months of age, neuron loss in the hippocampus is seen, becoming more severe in hippocampus, as well as amygdala, neocortex and entorhinal cortex by 12 months of age

neurodegeneration
- mice show progressive neurodegeneration starting at 1 month of age, as determined by increasing loss of synaptophysin immunoreactivity

neurofibrillary tangles
- at 6 months of age, neurofibrillary tangles (NFT) are evident in neocortex, amygdala, hippocampus, brain stem and spinal cord but none are found in mice expressing wild-type human MAPT up to 24 months of age
- mutants develop ThS-positive neurofibrillary tangles

reduced long term potentiation
- LTP in CA1 region of hippocampus is significantly deteriorated, indicating attenuated postsynaptic responsiveness and compromised synaptic plasticity, but at 6 months no overt reduction in neuron number is detected

tau protein deposits
- aggregation of insoluble tau in the cortex and hippocampus
- at 3 months of age, mutants and mice expressing wild-type transgenic human tau show weak perikaryal and dendritic tau staining mainly in hippocampus, amygdala, cortex, brain stem, and spinal cord; at 6 months, mutants show stronger tau-positive neuronal staining in the hippocampus, amygdala, and spinal cord but older mice expressing wild-type human tau protein show no increases up to 12 months
- mutants exhibit progression in the distribution of abnormally phosphorylated tau from the entorhinal and neocortex, followed by involvement of the hippocampal formation and subcortical structures, to finally penetration of all layers of the neocortex
- taining in the hippocampus, amygdala, and spinal cord but older mice expressing wild-type human tau protein show no increases up to 12 months
- with aging, brains of mice have increasing levels of insoluble tau deposits composed mainly of transgenic human tau; decrease in solubility of tau is observed between 3 and 6 months

References

Yoshiyama Y; Higuchi M; Zhang B; Huang SM; Iwata N; Saido TC; Maeda J; Suhara T; Trojanowski JQ; Lee VM. 2007. Synapse loss and microglial activation precede tangles in a P301S tauopathy mouse model. Neuron 53(3):337-51PubMed: 17270732 MGI: J:119741

Additional - Tg(Prnp-MAPT*P301S)PS19Vle related

Technical Support

Contact Technical Support

Genotyping Protocols
- Standard PCR: Tg(Prnp-MAPT*P301S)PS19Vle alternate2
- QPCR: Tg(Prnp-MAPT*P301S)PS19Vle QPCR
- High Resolution Melting: Tg(Prnp-MAPT*P301S)PS19Vle alternate2
- MELT: Tg(Prnp-MAPT*P301S)PS19Vle-Chr3
- Probe: Tg(Prnp-MAPT*P301S)PS19Vle-Chr3 Probe
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

When maintaining a live colony, these mice can be bred as hemizygotes. These mice cannot be bred to homozygosity as homozygous females do not mate.
- Additional Breeding and Husbandry Support
Mating System
- Hemizygote x Noncarrier
- Noncarrier x Hemizygote
Citation
When using the B6;C3-Tg(Prnp-MAPT*P301S)PS19Vle/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #008169 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX10 (Standard)

Pricing & Availability

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Live Mouse

Age

Genotype

Price

weeks

Breeder Pair

Sex

Genotype

Price

Female
Male

Cryorecovery - Pricing

Service	Genotype	Price
	Hemizygous or Non carrier for Tg(Prnp-MAPT*P301S)PS19Vle

We will fulfill your order by providing at least two carriers for each strain ordered. The total number, sex, and genotypes provided will vary, although typically 8 or more animals are provided. Please check genotypes which will be recovered. While the genotypes of all animals produced will be communicated to you prior to scheduling shipment, the genotypes of animals provided may not reflect the mating scheme and genotypes described in the strain description. Animals are typically ready to ship in 11-14 weeks. If a second recovery is required to produce the minimum number of animals, then delivery time would increase to approximately 25 weeks. If we fail to produce animals of the correct genotype, you will not be charged. We cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation.

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Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Expression Data

Control Suggestions

Approximate Controls

Additional Information

Selected References

Tg(Prnp-MAPT*P301S)PS19Vle

Allele Symbol: Tg(Prnp-MAPT*P301S)PS19Vle

Disease Terms

Characteristics of this human disease are associated with transgenes and other mutation types in the mouse.

Research Areas By Genotype

This mouse can be used to support research in many areas including:

Genotype: Tg(Prnp-MAPT*P301S)PS19Vle related

Mammalian Phenotype Terms by Genotype

Genotype: Tg(Prnp-MAPT*P301S)PS19Vle/0B6.Cg-Tg(Prnp-MAPT*P301S)PS19Vle

behavior/neurological phenotype

integument phenotype

nervous system phenotype

Genotype: Tg(Prnp-MAPT*P301S)PS19Vle/Tg(Prnp-MAPT*P301S)PS19Vleinvolves: C3H * C57BL/6

behavior/neurological phenotype

Genotype: Tg(Prnp-MAPT*P301S)PS19Vle/0involves: C3H * C57BL/6

behavior/neurological phenotype

growth/size/body region phenotype

mortality/aging

muscle phenotype

nervous system phenotype

References

Additional - Tg(Prnp-MAPT*P301S)PS19Vle related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Citation

Animal Health Reports

Live Mouse

Breeder Pair

Cryorecovery - Pricing

Related Products and Services

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms of Use

Additional Use Restrictions Apply

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

Genotype: Tg(Prnp-MAPTP301S)PS19Vle/0
B6.Cg-Tg(Prnp-MAPTP301S)PS19Vle

Genotype: Tg(Prnp-MAPTP301S)PS19Vle/Tg(Prnp-MAPTP301S)PS19Vle
involves: C3H * C57BL/6

Genotype: Tg(Prnp-MAPTP301S)PS19Vle/0
involves: C3H C57BL/6