Strain Name:

129-Cstbtm1Rm/J

Stock Number:

003486

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Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Specieslaboratory mouse
 
Donating InvestigatorDr. Richard M. Myers,   Stanford University School of Medicine

Description
The progressive myoclonus epilepsies (PMEs) types are diseases characterized by tonic-clonic seizures, myoclonic seizures and progressive neurological dysfunction, including dementia and ataxia. Mice lacking cystatin B develop myoclonic seizures and ataxia, similar to symptoms seen in one of these human diseases. Specifically, this mouse is a model of Unverricht-Lundborg disease (EPM1).Strain background has an effect on phenotype.

Development
To disrupt the gene, a Cstb targeting vector containing a 12.3 kb PGK-neo expression cassette was inserted into the EagI site in exon 1.

Control Information

  Control
   Wild-type from the colony
 
  Considerations for Choosing Controls

Additional Web Information

New 129 Nomenclature Bulletin

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Myoclonic Epilepsy of Unverricht and Lundborg
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Cstbtm1Rm/Cstbtm1Rm

        either: (involves: 129S1/Sv * 129X1/SvJ) or (involves: 129S1/Sv * 129X1/SvJ * C57BL/6)
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype
    • at 1-3 months of age, mutant mice displayed normal grooming behavior, coordination and strength   (MGI Ref ID J:50587)
    • abnormal gait
      • at >6 months, mutant mice walked with a wide-based gait and, upon hindlimb rearing, occasionally fell on their sides, but still displayed normal swimming ability   (MGI Ref ID J:50587)
    • ataxia
      • at 6 months, homozygous null mice showed mild signs of ataxia   (MGI Ref ID J:50587)
    • impaired coordination
      • at 7-9 months of age, mutant mice performed poorly on both the still and rotating rotorod   (MGI Ref ID J:50587)
    • myoclonus
      • isogenic 129/Sv mutant mice developed myoclonus and seizures during sleep by 1 month of age   (MGI Ref ID J:50587)
      • seizure episodes were typified by short twitching of either the whiskers, ears or tail, followed by facial spasms and minor shaking of the torso and limbs   (MGI Ref ID J:50587)
      • shaking became more prominent with intermittent lightning-like muscle jerks, sometimes propelling the animal forward   (MGI Ref ID J:50587)
      • each event lasted from a few seconds to several minutes, and ended with a large myoclonic outburst that catapulted the animal into the air   (MGI Ref ID J:50587)
      • after the seizure, animals remained still for several seconds, and finally regained mobility   (MGI Ref ID J:50587)
      • during sleep, the entire myoclonic seizure occurred often, sometimes every several minutes; seizures occurred only during sleep   (MGI Ref ID J:50587)
      • electrocortical graph recordings revealed abnormal cortical activity during the stereotyped behavioral seizures; seizure episodes correlated precisely (1:1) with the multifocal myoclonic activity   (MGI Ref ID J:50587)
      • recordings revealed a bilaterally synchronous 4-6-Hz repetitive spike discharge which coincided with the onset of the hyperkinetic behaviour; ECoG activity reverted to the normal non-spiking pattern upon regaining mobility   (MGI Ref ID J:50587)
      • isogenic 129/Sv mutant mice exhibited no photoconvulsive response following a 1-45-Hz photic stimulation   (MGI Ref ID J:50587)
      • ECoG recordings from awake homozygotes, or mutant mice on the mixed 129Sv x C57BL/6 genetic background, showed no identifiable cortical seizure patterns   (MGI Ref ID J:50587)
  • cellular phenotype
  • abnormal apoptosis
    • in addition to the decreased density of granule cells, all homozygotes contained numerous TUNEL-positive apoptotic cells in the granule cell layer of the cerebellum, regardless of their age   (MGI Ref ID J:50587)
    • notably, the cerebellum of pure 129X1/SvJ mutant mice contained ~2-fold more TUNEL-positive granule cells than age-matched mutants derived from the mixed 129Sv x C57BL/6 genetic background   (MGI Ref ID J:50587)
    • at 3 months, TEM analysis of cerebellar tissue from pure 129X1/SvJ homozygous null mice revealed that granule cells showed both early apoptotic cellular features, including chromatin marginization and nuclear condensation, and late apoptotic cellular features, including the presence of apoptotic bodies and cytoplasmic vacuoles   (MGI Ref ID J:50587)
  • growth/size/body phenotype
  • *normal* growth/size/body phenotype
    • homozygous null mice were viable and appeared phenotypically normal at 3 weeks prior to weaning   (MGI Ref ID J:50587)
    • at 1-3 months of age, mutant mice displayed normal size and weight relative to wild-type   (MGI Ref ID J:50587)
  • immune system phenotype
  • increased incidence of corneal inflammation
    • with increasing age, increased incidence of corneal inflammation was observed in the absence of bacterial or viral infections   (MGI Ref ID J:50587)
  • uveitis
    • a few corneal opacities were associated with anterior uveitis, i.e. accumulations of neutrophils in the anterior chamber   (MGI Ref ID J:50587)
  • muscle phenotype
  • myoclonus
    • isogenic 129/Sv mutant mice developed myoclonus and seizures during sleep by 1 month of age   (MGI Ref ID J:50587)
    • seizure episodes were typified by short twitching of either the whiskers, ears or tail, followed by facial spasms and minor shaking of the torso and limbs   (MGI Ref ID J:50587)
    • shaking became more prominent with intermittent lightning-like muscle jerks, sometimes propelling the animal forward   (MGI Ref ID J:50587)
    • each event lasted from a few seconds to several minutes, and ended with a large myoclonic outburst that catapulted the animal into the air   (MGI Ref ID J:50587)
    • after the seizure, animals remained still for several seconds, and finally regained mobility   (MGI Ref ID J:50587)
    • during sleep, the entire myoclonic seizure occurred often, sometimes every several minutes; seizures occurred only during sleep   (MGI Ref ID J:50587)
    • electrocortical graph recordings revealed abnormal cortical activity during the stereotyped behavioral seizures; seizure episodes correlated precisely (1:1) with the multifocal myoclonic activity   (MGI Ref ID J:50587)
    • recordings revealed a bilaterally synchronous 4-6-Hz repetitive spike discharge which coincided with the onset of the hyperkinetic behaviour; ECoG activity reverted to the normal non-spiking pattern upon regaining mobility   (MGI Ref ID J:50587)
    • isogenic 129/Sv mutant mice exhibited no photoconvulsive response following a 1-45-Hz photic stimulation   (MGI Ref ID J:50587)
    • ECoG recordings from awake homozygotes, or mutant mice on the mixed 129Sv x C57BL/6 genetic background, showed no identifiable cortical seizure patterns   (MGI Ref ID J:50587)
  • vision/eye phenotype
  • abnormal cornea morphology
    • the corneal epithelial layers appeared eroded, ulcerated, or hyperplastic and keratinized   (MGI Ref ID J:50587)
    • corneal opacity
      • as homozygous null mice aged from 3 to 7 months, 35% of mutants and 0% of wild-type littermates developed corneal opacity in one or both eyes; in 35% of the cases, both eyes were affected   (MGI Ref ID J:50587)
      • corneal opacities corresponded with histopathological lesions of acute to chronic keratitis   (MGI Ref ID J:50587)
    • increased incidence of corneal inflammation
      • with increasing age, increased incidence of corneal inflammation was observed in the absence of bacterial or viral infections   (MGI Ref ID J:50587)
  • abnormal eye physiology
    • at 1-3 months of age, approximately 40% of homozygous null mice displayed narrowed palpebral fissures (squinting), increased lacrimation (tearing) and periocular buildup of serous to mucoid exudate   (MGI Ref ID J:50587)
    • increased incidence of corneal inflammation
      • with increasing age, increased incidence of corneal inflammation was observed in the absence of bacterial or viral infections   (MGI Ref ID J:50587)
    • uveitis
      • a few corneal opacities were associated with anterior uveitis, i.e. accumulations of neutrophils in the anterior chamber   (MGI Ref ID J:50587)
  • nervous system phenotype
  • abnormal nervous system physiology
    • quantitative RT-PCR revealed significant increases in the transcript levels of several transcripts in neurological tissues from inbred 129X1/SvJ homozygous null mice   (MGI Ref ID J:71823)
    • myoclonus
      • isogenic 129/Sv mutant mice developed myoclonus and seizures during sleep by 1 month of age   (MGI Ref ID J:50587)
      • seizure episodes were typified by short twitching of either the whiskers, ears or tail, followed by facial spasms and minor shaking of the torso and limbs   (MGI Ref ID J:50587)
      • shaking became more prominent with intermittent lightning-like muscle jerks, sometimes propelling the animal forward   (MGI Ref ID J:50587)
      • each event lasted from a few seconds to several minutes, and ended with a large myoclonic outburst that catapulted the animal into the air   (MGI Ref ID J:50587)
      • after the seizure, animals remained still for several seconds, and finally regained mobility   (MGI Ref ID J:50587)
      • during sleep, the entire myoclonic seizure occurred often, sometimes every several minutes; seizures occurred only during sleep   (MGI Ref ID J:50587)
      • electrocortical graph recordings revealed abnormal cortical activity during the stereotyped behavioral seizures; seizure episodes correlated precisely (1:1) with the multifocal myoclonic activity   (MGI Ref ID J:50587)
      • recordings revealed a bilaterally synchronous 4-6-Hz repetitive spike discharge which coincided with the onset of the hyperkinetic behaviour; ECoG activity reverted to the normal non-spiking pattern upon regaining mobility   (MGI Ref ID J:50587)
      • isogenic 129/Sv mutant mice exhibited no photoconvulsive response following a 1-45-Hz photic stimulation   (MGI Ref ID J:50587)
      • ECoG recordings from awake homozygotes, or mutant mice on the mixed 129Sv x C57BL/6 genetic background, showed no identifiable cortical seizure patterns   (MGI Ref ID J:50587)
  • cerebellum hypoplasia
    • at 6-9 months, older homozygous null mice displayed a reduction in the density of the granule cell layer in the cerebellum   (MGI Ref ID J:50587)

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

Cstbtm1Rm/Cstbtm1Rm

        involves: 129S1/Sv * 129X1/SvJ * C57BL/6
  • behavior/neurological phenotype
  • ataxia
    • by 8 months of age, mice display ataxia   (MGI Ref ID J:115694)
  • seizures
    • occur during both sleep and wakefulness   (MGI Ref ID J:115694)
    • myoclonus
      • mice display frequent spontaneous axial myoclonic jerks at rate of 10-15/hour; head and neck are always involved, with whole body involved in most animals   (MGI Ref ID J:115694)
  • nervous system phenotype
  • abnormal brain wave pattern
    • baseline cortical activity displays normal low-amplitude desynchronized EEG with intermittent interictal discharges and bilateral electrographic seizure discharges   (MGI Ref ID J:115694)
  • abnormal cerebellum morphology
    • apoptosis is observed in cerebellum of mutants but not in wild-type brain at 4 months   (MGI Ref ID J:115694)
    • abnormal cerebellar granule cell morphology
      • widespread granule cell apoptosis is observed in mice at 2, 4, and 6 months of age   (MGI Ref ID J:115694)
  • seizures
    • occur during both sleep and wakefulness   (MGI Ref ID J:115694)
    • myoclonus
      • mice display frequent spontaneous axial myoclonic jerks at rate of 10-15/hour; head and neck are always involved, with whole body involved in most animals   (MGI Ref ID J:115694)
  • vision/eye phenotype
  • abnormal cornea morphology
    • at 8 months, around half of mutants may have serous exudate and or corneal lesions in one or both eyes   (MGI Ref ID J:115694)
    • corneal scarring
      • at 8 months, around half of mutants display a mild eye phenotype with corneal lesions and /or serous exudate in one or both eyes   (MGI Ref ID J:115694)
  • muscle phenotype
  • myoclonus
    • mice display frequent spontaneous axial myoclonic jerks at rate of 10-15/hour; head and neck are always involved, with whole body involved in most animals   (MGI Ref ID J:115694)
View Research Applications

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

Cstbtm1Rm related

Neurobiology Research
Ataxia (Movement) Defects
Cerebellar Defects
Epilepsy
Neurodegeneration

Sensorineural Research
Eye Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Cstbtm1Rm
Allele Name targeted mutation 1, Richard M Myers
Allele Type Targeted (Null/Knockout)
Common Name(s) Cystatin b-;
Mutation Made ByDr. Len Pennacchio,   Lawrence Berkeley National Laboratory
Strain of Origin(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
ES Cell Line NameR1
ES Cell Line Strain(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Gene Symbol and Name Cstb, cystatin B
Chromosome 10
Gene Common Name(s) AA960480; CST6; Cyb; EPM1; EPM1A; PME; STFB; Stfb; ULD; expressed sequence AA960480; stefin B (cystatin B);
Molecular Note A neomycin selection cassette was inserted into exon 1. Northern blot and RT-PCR analysis on RNA derived from liver of homozygous mice demonstrated that no detectable transcript was produced from this allele. Western blot analysis on extracts of brain tissue derived from homozygous mice confirmed that no detectable encoded protein was made. [MGI Ref ID J:50587]

Genotyping

Genotyping Information

Genotyping Protocols

Cstbtm1Rmalternate1,

Separated MCA


Cstbtm1Rm, Standard PCR
Cstbtm1Rmalternate1, Separated PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Pennacchio LA; Bouley DM; Higgins KM; Scott MP; Noebels JL; Myers RM. 1998. Progressive ataxia, myoclonic epilepsy and cerebellar apoptosis in cystatin B-deficient mice. Nat Genet 20(3):251-8. [PubMed: 9806543]  [MGI Ref ID J:50587]

Additional References

Cstbtm1Rm related

Butinar M; Prebanda MT; Rajkovic J; Jeric B; Stoka V; Peters C; Reinheckel T; Kruger A; Turk V; Turk B; Vasiljeva O. 2014. Stefin B deficiency reduces tumor growth via sensitization of tumor cells to oxidative stress in a breast cancer model. Oncogene 33(26):3392-400. [PubMed: 23955077]  [MGI Ref ID J:212612]

Ceru S; Konjar S; Maher K; Repnik U; Krizaj I; Bencina M; Renko M; Nepveu A; Zerovnik E; Turk B; Kopitar-Jerala N. 2010. Stefin B interacts with histones and cathepsin L in the nucleus. J Biol Chem 285(13):10078-86. [PubMed: 20075068]  [MGI Ref ID J:161079]

Franceschetti S; Sancini G; Buzzi A; Zucchini S; Paradiso B; Magnaghi G; Frassoni C; Chikhladze M; Avanzini G; Simonato M. 2007. A pathogenetic hypothesis of Unverricht-Lundborg disease onset and progression. Neurobiol Dis 25(3):675-85. [PubMed: 17188503]  [MGI Ref ID J:119089]

Houseweart MK; Vilaythong A; Yin XM; Turk B; Noebels JL; Myers RM. 2003. Apoptosis caused by cathepsins does not require Bid signaling in an in vivo model of progressive myoclonus epilepsy (EPM1). Cell Death Differ 10(12):1329-35. [PubMed: 12934064]  [MGI Ref ID J:115694]

Kaasik A; Kuum M; Aonurm A; Kalda A; Vaarmann A; Zharkovsky A. 2007. Seizures, ataxia, and neuronal loss in cystatin B heterozygous mice. Epilepsia 48(4):752-7. [PubMed: 17319918]  [MGI Ref ID J:147700]

Kaur G; Mohan P; Pawlik M; DeRosa S; Fajiculay J; Che S; Grubb A; Ginsberg SD; Nixon RA; Levy E. 2010. Cystatin C rescues degenerating neurons in a cystatin B-knockout mouse model of progressive myoclonus epilepsy. Am J Pathol 177(5):2256-67. [PubMed: 20889561]  [MGI Ref ID J:166252]

Lehtinen MK; Tegelberg S; Schipper H; Su H; Zukor H; Manninen O; Kopra O; Joensuu T; Hakala P; Bonni A; Lehesjoki AE. 2009. Cystatin B deficiency sensitizes neurons to oxidative stress in progressive myoclonus epilepsy, EPM1. J Neurosci 29(18):5910-5. [PubMed: 19420257]  [MGI Ref ID J:148480]

Lieuallen K; Pennacchio LA; Park M; Myers RM; Lennon GG. 2001. Cystatin B-deficient mice have increased expression of apoptosis and glial activation genes. Hum Mol Genet 10(18):1867-71. [PubMed: 11555622]  [MGI Ref ID J:71823]

Maher K; Zavrsnik J; Jeric-Kokelj B; Vasiljeva O; Turk B; Kopitar-Jerala N. 2014. Decreased IL-10 expression in stefin B-deficient macrophages is regulated by the MAP kinase and STAT-3 signaling pathways. FEBS Lett 588(5):720-6. [PubMed: 24462687]  [MGI Ref ID J:206662]

Shannon P; Pennacchio LA; Houseweart MK; Minassian BA; Myers RM. 2002. Neuropathological changes in a mouse model of progressive myoclonus epilepsy: cystatin B deficiency and Unverricht-Lundborg disease. J Neuropathol Exp Neurol 61(12):1085-91. [PubMed: 12484571]  [MGI Ref ID J:104999]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2525.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory 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. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $3283.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.

    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 10 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory 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. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

  Control
   Wild-type from the colony
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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