Overview

Also Known As:Tsc1 flox, Tsc1^c

These floxed mutant mice possess loxP sites flanking exons 17 and 18 of the Tsc1 gene. This mutant strain may be useful in tissue-specific studies including tuberous sclerosis or other hamartoma syndromes, regulation of the actin cytoskeleton and motility, cellular and organismal glucose homeostasis, cell growth responses, apoptosis regulation, and regulation of cell size.

Donating Investigator

David J. Kwiatkowski, Brigham and Women's Hospital

Genetic overview

Genetic Background	Generation
	?+N1pF2 (2020-01-20 00:00:00)

Tsc1^tm1Djk

Allele Type	Gene Symbol	Gene Name
Targeted (Conditional ready (e.g. floxed), No functional change)	Tsc1	tuberous sclerosis 1

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Research Applications

Research Tools

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Base Price

Starting at:

$255.00 Domestic price for female 4-week

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Details

Detailed Description

Homozygous mice are viable, fertile, normal in size, have normal expression of hamartin (the targeted gene's protein product), have no growth or behavioral defects, and are devoid of tumors through age 18 months. This mutant carries a "floxed" allele of the endogenous gene. When combined with a mutant carrying a Cre recombinase gene under the control of a promoter of interest, exons 17 and 18 of Tsc1 are deleted in the tissue of interest. This mutant may be useful in many tissue-specific studies including tuberous sclerosis or other hamartoma syndromes, regulation of the actin cytoskeleton and motility, cellular and organismal glucose homeostasis, cell growth responses, apoptosis regulation, and regulation of cell size.

When bred to a strain expressing Cre recombinase in neuronal cells (see Stock No. 003966 for example), this mutant mouse strain may be useful in studies of tuberous sclerosis.

When bred to a strain expressing Cre recombinase in oocytes of the primordial follicles (see Stock No. 011062 for example), this mutant mouse strain may be useful in studies of primordial follicle quiescence and activation.

When bred to a strain expressing Cre recombinase in liver (see Stock No. 003574 for example), this mutant mouse strain may be useful in studies of hepatic lipid metabolism.

Importation of this model was supported by the Tuberous Sclerosis Alliance.

Development

A targeting vector containing a loxP-flanked neomycin resistance-thymidine kinase gene cassette preceding exon 17 and a third loxP site downstream of exon 18 was electroporated into 129S4/SvJae derived J1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. Chimeric mice were backcrossed for germ-line transmission to C57BL/6J, BALB/cJ, or 129/SvJae mice. The resulting heterozygotes were intercrossed to produce homozygotes on a mixed background.

Control Suggestions

None Available

Additional Information

Considerations for Choosing Controls

Selected References

Kwiatkowski DJ; Zhang H; Bandura JL; Heiberger KM; Glogauer M; el-Hashemite N; Onda H. 2002. A mouse model of TSC1 reveals sex-dependent lethality from liver hemangiomas, and up-regulation of p70S6 kinase activity in Tsc1 null cells. Hum Mol Genet 11(5):525-34PubMed: 11875047 MGI: J:75243

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Genetics

Tsc1^tm1Djk

Allele Symbol: Tsc1^tm1Djk

Allele Name	targeted mutation 1, David J Kwiatkowski
Allele Type	Targeted (Conditional ready (e.g. floxed), No functional change)
Allele Synonym(s)	Tsc1^c; Tsc1^fl; Tsc1^flox; Tsc1^L; Tsc1^lox
Gene Symbol and Name	Tsc1, tuberous sclerosis 1
Gene Synonym(s)
Strain of Origin	129S4/SvJae
Chromosome	2
General Note	Phenotypic Similarity to Human Syndrome: Angiosarcoma/Lymphangiosarcoma J: 231316.
Molecular Note	A floxed neo-TK cassette was inserted into the intron preceding exon 17 and a third loxP site was introduced downstream of exon 18 by homologous recombination.
Mutations Made By	David Kwiatkowski, Brigham and Women's Hospital

Disease/Phenotype

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

tuberous sclerosis

Research Areas By Phenotype

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

Research Tools
- Cancer Research
  - Hamartoma Syndromes
- Cre-lox System
  - loxP-flanked Sequences

Mammalian Phenotype Terms by Genotype

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

Genotype: Tsc1^tm1Djk/Tsc1^tm1.1Djk Tg(Syn1-cre)671Jxm/0
involves: 129S4/SvJae * C57BL/6 * CBA

behavior/neurological phenotype

abnormal involuntary movement
- clasping behavior and tremor are significantly ameliorated by rapamycin/RAD001 treatment relative to untreated animals at 30, 60, and 100 days postnatal

abnormal limb posture
- at death, usually in third to fifth postnatal week, mice are found with extensor posture of fore- and hindlimbs

hunched posture
- develops by by third or fourth postnatal week

hyperactivity
- apparent by P10

hypoactivity
- mice show progressive decline in activity with limited mobility by third or fourth postnatal week

increased startle reflex
- apparent by P10

limb grasping
- display posterior limb-clasping behavior when lifted by tail

seizures
- after P21, suspension by the tail results in gentle spinning leading severe seizure activity, followed by bradycardia and death
- mice develop clinical seizures, spontaneous and some provoked in most part by physical simulation; both types of seizures are mild or severe
- severe seizures are characterized by brief behavioral arrest, followed by several seconds of clonic activity, followed by tonic extensor posturing of trunk and limbs for 15-45 seconds

sporadic seizures
- only mild seizures occur spontaneously, characterized by brief myoclonic jerking of head and torso

straub tail
- tail dorsiflexion is exhibited

tremors
- progressive high-frequency trunk and limb tremor apparent by P10

cellular phenotype

abnormal neuron differentiation
- in mutant brains, neurons appear to be still actively growing after P14-21, whereas wild-type neurons have stopped growing
- this may result in the hypomyelination, due to secondary myelination failure

growth/size/body region phenotype

slow postnatal weight gain
- after P5 until death, mutants fail to gain weight at same rate as controls; average maximum weight is 10 grams

mortality/aging

premature death
- discontinuation of drug treatment at P30 results in clinical symptom improvement for 1-2 weeks followed by clinical deterioration and death at 79 days for rapamycin-treated and 77 days for RAD001-treated mutants
- median survival of 35 days, with no survivors beyond 65 days
- mice treated with rapamycin or RAD001 (mTOR inhibitor) show 90-100% survival to 80 days of age compared to median survival of 33 days for untreated mutants

nervous system phenotype

abnormal brain morphology
- enlarged cells are seen outside cerebral cortex, in other parts of brain including thalamus, hypothalamus and brainstem
- Normal - no increased cell loss or degeneration is observed in regions containing anomalous enlarged cells

abnormal brain wave pattern
- interictal (seizure) 1-2 second bursts of high-amplitude 7-8 hertz spikes are observed with high frequency compared with controls; these are without obvious clinical correlate
- mice aged P21-48 display 3 types of electrographic abnormalities: short spike bursts observed in all mice examined, occasionally spontaneous period of desynchronization with electrodecrement and at low incidence, frequent high-amplitude sharp waves

abnormal cerebral cortex morphology
- laminar organization is less distinct than in the 6 cortical layers of controls
- mild cortical disorganization is observed in mutants with or without rapamycin treatment
- mutants display subset of enlarged pS6-positive cells at base of cortex and in cortical layer V; drug treatment results in marked reduction in size of enlarged cells
- unusually large cells are observed in all six layers in mutants, particularly in layer V; layer of enlarged cells is seen at gray-white matter border throughout cerebral cortex at P21

abnormal dendrite morphology
- in hippocampal neuron cultures, neuronal dendritic spine density is reduced >20% compared to controls
- with rapamycin treatment, spine density is marginally increased; spine length however is increased 9% compared to treated and untreated controls or untreated mutants

abnormal dentate gyrus morphology
- enlarged cells are observed in hilus

abnormal hippocampus pyramidal cell layer
- enlarged cells are seen throughout pyramidal cell layer, particularly in CA3 region

abnormal hippocampus region morphology
- enlarged ectopic cells are seen outside the CA1-CA3 fields in stratum oriens and stratum radiatum

abnormal myelination
- hypomyelination is observed in brains of mutants
- myelination particularly in cortex is impaired due to decreased myelin production by oligodendrocytes; rapamycin treatment works to restore myelination throughout brain with greatest improvement in cortex and hippocampus
- Normal - oligodendrocyte number and distribution appears similar to wild-type

abnormal neocortex morphology
- contains some enlarged cells

abnormal neuron differentiation
- in mutant brains, neurons appear to be still actively growing after P14-21, whereas wild-type neurons have stopped growing
- this may result in the hypomyelination, due to secondary myelination failure

abnormal neuron morphology
- d at P7 does not significantly decrease abnormally oriented dendrite percentage
- in somatosensory cortex, layer V neurons often have major dendrites extending tangentially and diagonally to the pia, in contrast to control neurons which mainly have long apical dendrite oriented directly toward pial surface; rapamycin treatment initiated at P7 does not significantly decrease abnormally oriented dendrite percentage
- many pyramidal neurons demonstrate dysplastic features including increased size and thicker dendritic arbors compared to control neurons
- Nissl bodies and filamentous aggregates are often detected in enlarged neurons, prominently in brainstem but rarely in enlarged cortical cells
- population of neurons in lateral somatosensory cortex are considerably enlarged compared with those in controls; size is significantly reduced after drug treatment (from 1.8-fold to 1.2-fold), but effect reverses when treatment is stopped
- some neurons are aberrantly localized outside primary pyramidal cell layers; ectopic neurons are isolated, not organized into clusters or columns
- some neurons in somatosensory cortex show 60% increase in soma size relative to controls

increased brain weight
- brain weight to body weight ratio is significantly greater (2.4-fold) in mutants compared to wild-type; with rapamycin/RAD001 treatment, difference from control is significantly reduced but still observed

seizures
- after P21, suspension by the tail results in gentle spinning leading severe seizure activity, followed by bradycardia and death
- mice develop clinical seizures, spontaneous and some provoked in most part by physical simulation; both types of seizures are mild or severe
- severe seizures are characterized by brief behavioral arrest, followed by several seconds of clonic activity, followed by tonic extensor posturing of trunk and limbs for 15-45 seconds

sporadic seizures
- only mild seizures occur spontaneously, characterized by brief myoclonic jerking of head and torso

skeleton phenotype

abnormal spine curvature
- kyphosis is significantly improved in rapamycin/RAD001-treated mice compared with untreated mutants

Genotype: Tsc1^tm1Djk/Tsc1^tm1Djk Tg(Syn1-cre)671Jxm/0
involves: 129S4/SvJae * C57BL/6 * CBA

behavior/neurological phenotype

abnormal behavior

growth/size/body region phenotype

abnormal body size

mortality/aging

premature death
- Tg(Syn1-cre)671Jxm conditional mutants; however no data are presented
- clinical features, survival, and brain pathology are stated to be identical to that of Tsc1^tm1Djk Tsc1^tm1.1Djk Tg(Syn1-cre)671Jxm conditional mutants; however no data are presented

nervous system phenotype

abnormal nervous system morphology

abnormal nervous system physiology

Genotype: Tsc1^tm1Djk/Tsc1^tm1Djk
involves: 129S4/SvJae * C57BL/6

behavior/neurological phenotype

hypoactivity
- in fasted cre injected mice

growth/size/body region phenotype

enlarged liver
- about a 40% increase in liver mass following adenoviral cre retro-orbital injection

homeostasis/metabolism phenotype

decreased body temperature
- in fasted cre injected mice

decreased circulating ketone body level
- markedly lower serum ketones in young fasted cre injected mice but not in aged fasted cre injected mice

liver/biliary system phenotype

abnormal hepatocyte morphology
- increase in hepatocyte size following adenoviral cre retro-orbital injection

abnormal liver physiology
- cre injected mice are unable to generate ketones when given sodium octanoate
- decrease in liver protein content following adenoviral cre retro-orbital injection
- in cre injected mice, the liver is largely refractory to fast induced shrinkage

enlarged liver
- about a 40% increase in liver mass following adenoviral cre retro-orbital injection

Genotype: Tsc1^tm1Djk/Tsc1^tm1Djk Tg(Gdf9-icre)5092Coo/?
involves: 129S4/SvJae * C57BL/6J

endocrine/exocrine gland phenotype

abnormal ovarian follicle morphology
- injection with rapamycin reverses the overactivation of primordial follicles, indicative that mTORC1 activity is responsible for increased activation of follicles
- mutants exhibit premature activation of the entire primordial follicle pool by P23, leading to follicle depletion and premature ovarian failure in early adulthood (2-3 months of age)

premature ovarian failure
- premature ovarian failure in early adulthood (2-3 months of age)

homeostasis/metabolism phenotype

increased circulating follicle stimulating hormone level
- higher levels at 3-4 months of age

increased circulating luteinizing hormone level
- higher levels at 3-4 months of age

mortality/aging

premature ovarian failure
- premature ovarian failure in early adulthood (2-3 months of age)

reproductive system phenotype

abnormal ovarian follicle morphology
- injection with rapamycin reverses the overactivation of primordial follicles, indicative that mTORC1 activity is responsible for increased activation of follicles
- mutants exhibit premature activation of the entire primordial follicle pool by P23, leading to follicle depletion and premature ovarian failure in early adulthood (2-3 months of age)

premature ovarian failure
- premature ovarian failure in early adulthood (2-3 months of age)

reduced female fertility
- from 6-27 weeks of age, females produce at most 2 litters of normal size and then become infertile after around 12-13 weeks

Genotype: Tsc1^tm1Djk/Tsc1^tm1Djk Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺
involves: 129S4/SvJae * C57BL/6 * DBA

growth/size/body region phenotype

enlarged liver
- mutants develop hepatomegaly

mammalian phenotype

liver/biliary system phenotype
- Normal - mutants normally do not exhibit hepatic steatosis, however when fed a high-fat diet and treated with rapamycin, they develop steatosis and show increased levels of hepatic triglycerides

homeostasis/metabolism phenotype

abnormal homeostasis
- gene expression analysis indicates that fat utilization and glucose production are promoted in mutants

decreased circulating triglyceride level
- mutants do not show an increase in plasma triglyceride levels in response to the high-fat diet as is seen in wild-type mice
- plasma triglyceride levels are lower than in wild-type mice, however adiponectin and leptin levels are no different

impaired glucose tolerance
- mutants exhibit mild but significant glucose intolerance

insulin resistance
- Normal - however, fasting plasma glucose and insulin levels are normal
- insulin levels at 30 minutes following glucose administration are higher in mutants than controls, indicating insulin resistance
- mutants exhibit a slight reduction in systemic insulin sensitivity

liver/biliary system phenotype

abnormal hepatocyte morphology
- increase in hepatocyte cell size

abnormal hepatocyte physiology
- hepatocytes are resistant to steatosis induced by a high-fat diet

enlarged liver
- mutants develop hepatomegaly

Genotype: Tsc1^tm1Djk/Tsc1^tm1Djk
involves: 129S4/SvJae

mammalian phenotype

neoplasm
- Normal - mice do not develop mesothelioma following injection of adenovirus expressing Cre into the bladder or intraperitoneally at 2-3 months of age

Genotype: Tsc1^tm1Djk/Tsc1⁺ Tg(Pcp2-cre)2Mpin/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * BALB/cJ * C57BL/6J

behavior/neurological phenotype

abnormal response to novel odor
- Normal - however, mice show normal investigation of non-social olfactory cues
- mice show reduced investigation of social odors compared with controls, suggesting impaired discrimination of social olfactory cues

abnormal sexual interaction
- mice show impaired male-female social interactions, with reductions in the time that mice spend interacting compared to controls

abnormal social investigation
- in a 3-chambered assay of social approach and preference for social novelty, mice exhibit social impairments, showing no differences between the time spend in the chamber or in interaction with the novel mouse versus the novel object unlike controls
- in a social novelty paradigm, mice show no preference for social novelty

excessive vocalization
- P5-P12 pups show increased vocalizations

increased grooming behavior
- increase in self-grooming rates

nervous system phenotype

abnormal nervous system physiology
- despite receiving normal functioning synaptic inputs, the output of the cerebellar cortex is reduced, both tonically and in response to incoming excitatory drive
- injection of small hyperpolarizing currents results in smaller voltage changes in Purkinje cells, indicating a decrease in the effective input resistance
- Purkinje cell excitability is reduced, with Purkinje cells showing lower, graded spontaneous spiking rate, and current injection evokes fewer action potentials in Purkinje cells

abnormal Purkinje cell dendrite morphology
- increase in spine density on Purkinje cell dendrites

Genotype: Tsc1^tm1Djk/Tsc1^tm1Djk Tg(Pcp2-cre)2Mpin/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * BALB/cJ * C57BL/6J

behavior/neurological phenotype

abnormal learning/memory/conditioning
- mice exhibit similar acquisition learning of a submerged escape-platform location compared to controls, however when the escape platform location is reversed, mutants show impaired learning of the new platform location
- rapamycin treatment prevents the reversal learning impairment

abnormal response to novel odor
- Normal - however, mice show normal investigation of non-social olfactory cues
- mice show reduced investigation of social odors compared with controls, suggesting impaired discrimination of social olfactory cues

abnormal sexual interaction
- mice show impaired male-female social interactions, with reductions in the time that mice spend interacting compared to controls

abnormal social investigation
- in a 3-chambered assay of social approach and preference for social novelty, mice show social impairments, showing no differences between the time spend in the chamber or in interaction with the novel mouse versus the novel object
- in a social novelty paradigm, mice show no preference for social novelty
- treatment with rapamycin results in normal social behavior

ataxia
- mice show decreased stride length and increased stride width at 4 months of age
- mutants show initial signs of ataxia at 7-8 weeks of age which progresses with age
- rapamycin treated mutants do not show ataxic gait

excessive vocalization
- P5-P12 pups show increased vocalizations

impaired coordination
- mutants show impaired motor learning on the accelerating rotarod test before ataxia onset
- treatment with rapamycin prevents the motor phenotypes

increased grooming behavior
- increase in self-grooming rates

short stride length

nervous system phenotype

abnormal cerebellar Purkinje cell layer
- cerebellar Purkinje cell layer is abnormal with increased soma area and reduced Purkinje cell numbers
- treatment with rapamycin starting at P7 prevents the Purkinje cell defects

abnormal nervous system physiology
- despite receiving normal functioning synaptic inputs, the output of the cerebellar cortex is reduced, both tonically and in response to incoming excitatory drive
- Normal - however, alterations in synaptic transmission are not apparent in mutants
- injection of small hyperpolarizing currents results in smaller voltage changes in Purkinje cells, indicating a decrease in the effective input resistance
- Purkinje cell excitability is reduced, with Purkinje cells showing lower, graded spontaneous spiking rate, and current injection evokes fewer action potentials in Purkinje cells

abnormal Purkinje cell dendrite morphology
- increase in spine density on Purkinje cell dendrites

abnormal Purkinje cell morphology
- markers for endoplasmic reticulum and oxidative stress are elevated indicating elevated neuronal stress of Purkinje cells
- Purkinje cell soma area is increased at 4 weeks of age
- Purkinje cells display abnormal axonal projections with numerous protrusions and abnormal collateralization

decreased Purkinje cell number
- an increase in Purkinje cell apoptosis is seen at 7-8 weeks of age
- decrease in Purkinje cell numbers are first seen at 2 months of age, with a further reduction at 4 months

References

Kwiatkowski DJ; Zhang H; Bandura JL; Heiberger KM; Glogauer M; el-Hashemite N; Onda H. 2002. A mouse model of TSC1 reveals sex-dependent lethality from liver hemangiomas, and up-regulation of p70S6 kinase activity in Tsc1 null cells. Hum Mol Genet 11(5):525-34PubMed: 11875047 MGI: J:75243

Additional References

Asrani K; Murali S; Lam B; Na CH; Phatak P; Sood A; Kaur H; Khan Z; Noe M; Anchoori RK; Talbot CC Jr; Smith B; Skaro M; Lotan TL. 2019. mTORC1 feedback to AKT modulates lysosomal biogenesis through MiT/TFE regulation. J Clin Invest 129(12):5584-5599PubMed: 31527310 MGI: J:293727

Additional - Tsc1^tm1Djk related

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CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Standard PCR:Tsc1
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Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

When maintaining a live colony, these mice are maintained as homozygotes.
- Additional Breeding and Husbandry Support
Mating System
- Homozygote x Homozygote
Citation
When using the Tsc1^c mouse strain in a publication, please cite the originating article(s) and include JAX stock #005680 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX10 (Standard)

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	Heterozygous for Tsc1<tm1Djk>

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Also Known As:Tsc1 flox, Tsc1c

Donating Investigator

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Tsc1tm1Djk

Allele Symbol: Tsc1tm1Djk

Disease Terms

Models with phenotypic similarity to human diseases where etiology is unknown or involving genes where ortholog is unknown.

Research Areas By Phenotype

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

Mammalian Phenotype Terms by Genotype

Genotype: Tsc1tm1Djk/Tsc1tm1.1Djk Tg(Syn1-cre)671Jxm/0involves: 129S4/SvJae * C57BL/6 * CBA

behavior/neurological phenotype

cellular phenotype

growth/size/body region phenotype

mortality/aging

nervous system phenotype

skeleton phenotype

Genotype: Tsc1tm1Djk/Tsc1tm1Djk Tg(Syn1-cre)671Jxm/0involves: 129S4/SvJae * C57BL/6 * CBA

behavior/neurological phenotype

growth/size/body region phenotype

mortality/aging

nervous system phenotype

Genotype: Tsc1tm1Djk/Tsc1tm1Djkinvolves: 129S4/SvJae * C57BL/6

behavior/neurological phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

liver/biliary system phenotype

Genotype: Tsc1tm1Djk/Tsc1tm1Djk Tg(Gdf9-icre)5092Coo/?involves: 129S4/SvJae * C57BL/6J

endocrine/exocrine gland phenotype

homeostasis/metabolism phenotype

mortality/aging

reproductive system phenotype

Genotype: Tsc1tm1Djk/Tsc1tm1Djk Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+involves: 129S4/SvJae * C57BL/6 * DBA

growth/size/body region phenotype

mammalian phenotype

homeostasis/metabolism phenotype

liver/biliary system phenotype

Genotype: Tsc1tm1Djk/Tsc1tm1Djkinvolves: 129S4/SvJae

mammalian phenotype

Genotype: Tsc1tm1Djk/Tsc1+ Tg(Pcp2-cre)2Mpin/0involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * BALB/cJ * C57BL/6J

behavior/neurological phenotype

nervous system phenotype

Genotype: Tsc1tm1Djk/Tsc1tm1Djk Tg(Pcp2-cre)2Mpin/0involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * BALB/cJ * C57BL/6J

behavior/neurological phenotype

nervous system phenotype

References

Additional References

Additional - Tsc1tm1Djk related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Citation

Animal Health Reports

Live Mouse

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

Also Known As:Tsc1 flox, Tsc1^c

Tsc1^tm1Djk

Allele Symbol: Tsc1^tm1Djk

Genotype: Tsc1^tm1Djk/Tsc1^tm1.1Djk Tg(Syn1-cre)671Jxm/0
involves: 129S4/SvJae * C57BL/6 * CBA

Genotype: Tsc1^tm1Djk/Tsc1^tm1Djk Tg(Syn1-cre)671Jxm/0
involves: 129S4/SvJae * C57BL/6 * CBA

Genotype: Tsc1^tm1Djk/Tsc1^tm1Djk
involves: 129S4/SvJae * C57BL/6

Genotype: Tsc1^tm1Djk/Tsc1^tm1Djk Tg(Gdf9-icre)5092Coo/?
involves: 129S4/SvJae * C57BL/6J

Genotype: Tsc1^tm1Djk/Tsc1^tm1Djk Speer6-ps1^{Tg(Alb-cre)21Mgn}/Speer6-ps1⁺
involves: 129S4/SvJae * C57BL/6 * DBA

Genotype: Tsc1^tm1Djk/Tsc1^tm1Djk
involves: 129S4/SvJae

Genotype: Tsc1^tm1Djk/Tsc1⁺ Tg(Pcp2-cre)2Mpin/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * BALB/cJ * C57BL/6J

Genotype: Tsc1^tm1Djk/Tsc1^tm1Djk Tg(Pcp2-cre)2Mpin/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * BALB/cJ * C57BL/6J

Additional - Tsc1^tm1Djk related