Description

Strain Information

Type Congenic; Mutant Strain; Additional information on Genetically Engineered Mutant Mice. Species laboratory mouse Background Strain AKR/J Donor Strain C57BL/6.KB2/Rn Generation N13F4p (27-JUN-04)

Appearance
albino
Related Genotype: a/a Tyr^c/Tyr^c

Control Information

	Control
	Heterozygote from the colony
Considerations for Choosing Controls

Related Strains

Strains carrying   Cln8^mnd allele

001612

B6.KB2-Cln8mnd/MsrJ

View Strains carrying   Cln8^mnd     (1 strain)

Additional Web Information

Congenic Nomenclature

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms

Ceroid Lipofuscinosis, Neuronal, 8; CLN8 - Models with phenotypic similarity to human disease where etiologies involve orthologs.1

1 Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

View Mammalian Phenotype Terms

Mammalian Phenotype Terms

      assigned by genotype

Cln8^mnd/Cln8^mnd

        AK.B6(Cg)-Cln8^mnd

• life span-post-weaning/aging
• premature death (MGI Ref ID J:56219)
  • die by 5.5 months of age
• nervous system phenotype
• abnormal motor neuron morphology (MGI Ref ID J:56219)
  • motor neuron disease is accelerated even more than in the mixed AKR/J and B6.KB2 background, with symptoms appearing by 4 months and death by 5.5 months of age

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Cln8^mnd/Cln8⁺

        involves: B6.KB2 * C57BL/6Fla

• nervous system phenotype
• abnormal motor neuron morphology (MGI Ref ID J:8492)
  • exhibit neurological disease, with onset of mild symptoms at an age (5 months) similar to homozygotes
  • slower emergence of more severe motor neuron disease symptoms than in homozygotes

Cln8^mnd/Cln8^mnd

        B6.KB2/Rn-Cln8^mnd

• life span-post-weaning/aging
• premature death (MGI Ref ID J:56219)
  • most die by 9-14 months of age
• behavior/neurological phenotype
• abnormal motor capabilities/coordination/movement (MGI Ref ID J:8492)
  • hindlimbs are unable to grasp the bars of wire cagetop when attempting to walk over it
• abnormal locomotor activity (MGI Ref ID J:8492)
  • unable to walk uphill
  • dragging or splaying of the hindlimbs while walking
• ataxia (MGI Ref ID J:8492)
  • age of onset is approximately 5- 11 months of age, progressive with age
• limb grasping (MGI Ref ID J:8492)
• paralysis (MGI Ref ID J:12816)
  • progress to severe spastic paresis and paralysis by 9 months of age
• hindlimb paralysis (MGI Ref ID J:8492)
  • age of onset is approximately 5- 11 months of age, progressive with age
• paresis (MGI Ref ID J:12816)
  • begin to develop paresis by 6 months of age
• nervous system phenotype
• abnormal nervous system morphology (MGI Ref ID J:12816)
  • contain LFB-positive intracytoplasmic inclusion material in most neurons in virtually all parts of the brain and spinal cord unlike in controls
• abnormal anterior horn morphology (MGI Ref ID J:8492)
  • degeneration of anterior horn cells in the spinal cord
• abnormal cranial nerve morphology (MGI Ref ID J:8492)
  • degeneration of cranial nerves
• abnormal hypoglossal nerve morphology (MGI Ref ID J:8492)
  • degenerating
• abnormal vagus nerve morphology (MGI Ref ID J:8492)
  • degenerating dorsal motor vagus
• abnormal motor neuron morphology (MGI Ref ID J:8492)
  • inclusion bodies containing ubiquitin were found in spinal neurons of mnd mice, even prior to onset of symptoms
  • motor neurons have eccentric or indiscrete nuclei, disrupted membranes and shape changes
  • exhibit motor neuron disease symptoms at around 6 months of age
• motor neuron degeneration (MGI Ref ID J:8492)
  • degeneration of the upper and lower motor neurons of the spinal cord and cranial nerves and of some areas of the brain
• reproductive system phenotype
• decreased litter size (MGI Ref ID J:8492)
  • lower number of progeny/litter and lower numbers of total litters
• vision/eye phenotype
• abnormal retinal photoreceptor layer (MGI Ref ID J:12816)
  • atrophy of the photoreceptor layer in mice older than 3 months and nearly complete loss of this layer by 8 months of age
• blindness (MGI Ref ID J:12816)
  • begin to become blind by 2 months of age and by 5 months, are completely blind

Cln8^mnd/Cln8^mnd

        involves: AKR/J * B6.KB2

• life span-post-weaning/aging
• premature death (MGI Ref ID J:56219)
  • death by 7 months of age, compared to 9-14 months on the inbred B6.KB2 background
• vision/eye phenotype
• abnormal retinal photoreceptor layer (MGI Ref ID J:19328)
• abnormal retinal rod cell inner segment morphology (MGI Ref ID J:19328)
  • rapid thinning of the rod inner segment layer by P25, with a more gradual thinning at later stages
• abnormal retinal rod cell outer segment morphology (MGI Ref ID J:19328)
  • rapid thinning of the rod outer segment layer by P25, with a more gradual thinning at later stages
• short photoreceptor inner segment (MGI Ref ID J:19328)
  • at very late stages of degeneration, inner segments are shortened and broadened
• short photoreceptor outer segment (MGI Ref ID J:19328)
  • progressive shortening of the outer segments while maintaining relatively normal structure
• abnormal retinal pigment epithelium morphology (MGI Ref ID J:19328)
  • focal thinning of the retinal pigment epithelium occurs at late stages of degeneration
• retinal degeneration (MGI Ref ID J:19328)
  • detectable at P15 and more pronounced with age
• thin retinal outer nuclear layer (MGI Ref ID J:19328)
  • at P15, the outer nuclear layer (ONL) contains greater number of pyknotic nuclei and is thinner
  • rapid thinning of the ONL by P25, with a more gradual thinning at later ages
• pigmentation phenotype
• abnormal retinal pigment epithelium morphology (MGI Ref ID J:19328)
  • focal thinning of the retinal pigment epithelium occurs at late stages of degeneration
• nervous system phenotype
• abnormal nervous system morphology (MGI Ref ID J:1224)
  • earlier age of onset (4.5-5 months) and increased speed of progression of neurological disease than on the inbred B6.KB2 background
• abnormal motor neuron morphology (MGI Ref ID J:56219)
  • motor neuron disease is accelerated with 40% exhibiting symptoms by 4.5 months of age and dying by 6.5-7 months
• abnormal retinal rod cell inner segment morphology (MGI Ref ID J:19328)
  • rapid thinning of the rod inner segment layer by P25, with a more gradual thinning at later stages
• abnormal retinal rod cell outer segment morphology (MGI Ref ID J:19328)
  • rapid thinning of the rod outer segment layer by P25, with a more gradual thinning at later stages
• short photoreceptor inner segment (MGI Ref ID J:19328)
  • at very late stages of degeneration, inner segments are shortened and broadened
• short photoreceptor outer segment (MGI Ref ID J:19328)
  • progressive shortening of the outer segments while maintaining relatively normal structure

Cln8^mnd/Cln8^mnd

        involves: B6.KB2 * C3H/HeJ

• life span-post-weaning/aging
• premature death (MGI Ref ID J:56219)
  • death similar to that seen on the inbred B6.KB2 background
• nervous system phenotype
• abnormal nervous system morphology (MGI Ref ID J:1224)
  • neurological disease progresses in a similar fashion as on the inbred B6.KB2 background
• abnormal motor neuron morphology (MGI Ref ID J:56219)
  • exhibit motor neuron disease symptoms at around 6 months of age and do not die prior to 10-12 months of age

Cln8^mnd/Cln8^mnd

        involves: B6.KB2

• nervous system phenotype
• abnormal myelination (MGI Ref ID J:47292)
  • many profiles of degenerating myelin sheaths and axons are seen in the white matter of the spinal cord
  • lesions in the spinal cord are consistent with Wallerian degeneration
• axon degeneration (MGI Ref ID J:47292)
  • many profiles of degenerating myelin sheaths and axons are seen in the white matter of the spinal cord
  • lesions in the spinal cord are consistent with Wallerian degeneration
  • however, no necrotic or apoptotic nuclei are detected in the central nervous system
• gliosis (MGI Ref ID J:47292)
• seizures (MGI Ref ID J:47292)
  • terminal seizures have been seen
• behavior/neurological phenotype
• seizures (MGI Ref ID J:47292)
  • terminal seizures have been seen

View Research Applications

Research Applications

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

Cln8^mnd related

Neurobiology Research
Ataxia (Movement) Defects
Behavioral and Learning Defects
Metabolic Defects
Neurodegeneration
Neuromuscular Defects

Sensorineural Research
Retinal Degeneration

Genes & Alleles

Gene & Allele Information

Allele Symbol		Cln8mnd
Allele Name		motor neuron degeneration
Allele Type		Spontaneous
Common Name(s)		Cln8mnd; mnd;
Strain of Origin		B6.KB2-H2b5
Gene Symbol and Name		Cln8, ceroid-lipofuscinosis, neuronal 8
Chromosome		8
Gene Common Name(s)		C8orf61; EPMR; FLJ39417; MGC93871; mnd; motor neuron degeneration;
General Note		It was originally thought that heterozygotes (mnd/+) could be detected at very old ages. However, it has been impossible to repeat these results and, even in 18-month old heterozygotes, no histological pathology is detectable (A. Messer and R. Bronson, personal communication, 1993). Early papers (J:8492, J:1224) state that this allele exhibits phenotypic similarity to amytrophic lateral sclerosis (ALS), however further analysis (J:12816, 56219) revealed that it is a better model for neuronal ceroid lipofuscinoses (Batten's disease) than for ALS.
Molecular Note		A single nucleotide insertion (267-268C, codon 90) predicts a frameshift and a truncated protein. [MGI Ref ID J:57766]

Genotyping

Genotyping Information

Genotyping Protocols

Cln8^mnd, STD PCR, vers. 1

Helpful Links

Optimizing PCR Protocols

References

References

Additional References

Cln8^mnd related

Bakalian A; Kopmels B; Messer A; Fradelizi D; Delhaye-Bouchaud N; Wollman E; Mariani J. 1992. Peripheral macrophage abnormalities in mutant mice with spinocerebellar degeneration. Res Immunol 143(1):129-39. [PubMed: 1565842]  [MGI Ref ID J:2228]

Battaglioli G; Martin DL; Plummer J; Messer A. 1993. Synaptosomal glutamate uptake declines progressively in the spinal cord of a mutant mouse with motor neuron disease. J Neurochem 60(4):1567-9. [PubMed: 8095977]  [MGI Ref ID J:4191]

Bennett MJ; Boriack RL; Birch DG. 1997. In-utero and post-delivery supplementation of motor neuron degeneration mutant mice with polyunsaturated fatty acids does not alter the clinical or pathological course. Neuropediatrics 28(1):82-4. [PubMed: 9151333]  [MGI Ref ID J:42641]

Bermingham NA; Martin JE; Fisher EM. 1996. The mouse lysosomal membrane protein 1 gene as a candidate for the motorneuron degeneration (mnd) locus. Genomics 32(2):266-71. [PubMed: 8833154]  [MGI Ref ID J:31840]

Bertamini M; Marzani B; Guarneri R; Guarneri P; Bigini P; Mennini T; Curti D. 2002. Mitochondrial oxidative metabolism in motor neuron degeneration (mnd) mouse central nervous system. Eur J Neurosci 16(12):2291-6. [PubMed: 12492423]  [MGI Ref ID J:108072]

Bihl F; Lariviere L; Qureshi ST; Flaherty L; Malo D. 2001. LPS-hyporesponsiveness of mnd mice is associated with a mutation in Toll-like receptor 4. Genes Immun 2(1):56-9. [PubMed: 11294571]  [MGI Ref ID J:103167]

Bolivar VJ; Scott Ganus J; Messer A. 2002. The development of behavioral abnormalities in the motor neuron degeneration (mnd) mouse. Brain Res 937(1-2):74-82. [PubMed: 12020865]  [MGI Ref ID J:107789]

Boyce S; Webb JK; Carlson E; Rupniak NM; Hill RG; Martin JE. 1999. Onset and progression of motor deficits in motor neuron degeneration (mnd) mice are unaltered by the glycine/NMDA receptor antagonist L-701,324 or the MAO-B inhibitor R(-)-deprenyl. Exp Neurol 155(1):49-58. [PubMed: 9918704]  [MGI Ref ID J:52561]

Bronson RT; Donahue LR; Johnson KR; Tanner A; Lane PW; Faust JR. 1998. Neuronal ceroid lipofuscinosis (nclf), a new disorder of the mouse linked to chromosome 9. Am J Med Genet 77(4):289-97. [PubMed: 9600738]  [MGI Ref ID J:47292]

Bronson RT; Lake BD; Cook S; Taylor S; Davisson MT. 1993. Motor neuron degeneration of mice is a model of neuronal ceroid lipofuscinosis (Batten's disease). Ann Neurol 33(4):381-5. [PubMed: 7683855]  [MGI Ref ID J:12816]

Callahan LM; Wylen EL; Messer A; Mazurkiewicz JE. 1991. Neurofilament distribution is altered in the Mnd (motor neuron degeneration) mouse. J Neuropathol Exp Neurol 50(4):491-504. [PubMed: 2061715]  [MGI Ref ID J:121249]

Chang B; Bronson RT; Hawes NL; Roderick TH; Peng C; Hageman GS; Heckenlively JR. 1994. Retinal degeneration in motor neuron degeneration: a mouse model of ceroid lipofuscinosis. Invest Ophthalmol Vis Sci 35(3):1071-6. [PubMed: 8125718]  [MGI Ref ID J:17934]

Chang B; Hawes NL; Hurd RE; Davisson MT; Nusinowitz S; Heckenlively JR. 2002. Retinal degeneration mutants in the mouse. Vision Res 42(4):517-25. [PubMed: 11853768]  [MGI Ref ID J:75095]

Cho SK; Gao N; Pearce DA; Lehrman MA; Hofmann SL. 2005. Characterization of lipid-linked oligosaccharide accumulation in mouse models of Batten disease. Glycobiology 15(6):637-48. [PubMed: 15647513]  [MGI Ref ID J:112499]

Cook S; Davisson MT; Bronson R; Messer A. 1993. New mutation - motor neuron degeneration - mnd Mouse Genome 91(2):313.  [MGI Ref ID J:29019]

Cooper JD; Messer A; Feng AK; Chua-Couzens J; Mobley WC. 1999. Apparent loss and hypertrophy of interneurons in a mouse model of neuronal ceroid lipofuscinosis: evidence for partial response to insulin-like growth factor-1 treatment. J Neurosci 19(7):2556-67. [PubMed: 10087069]  [MGI Ref ID J:53928]

Faust JR; Rodman JS; Daniel PF; Dice JF; Bronson RT. 1994. Two related proteolipids and dolichol-linked oligosaccharides accumulate in motor neuron degeneration mice (mnd/mnd), a model for neuronal ceroid lipofuscinosis. J Biol Chem 269(13):10150-5. [PubMed: 8144516]  [MGI Ref ID J:17522]

Fujita K; Shibayama K; Yamauchi M; Kato T; Ando M; Takahashi H; Iritani K; Yoshimoto N; Nagata Y. 1998. Alteration of enzymatic activities implicating neuronal degeneration in the spinal cord of the development. Neurochem Res 23(4):557-62. [PubMed: 9566592]  [MGI Ref ID J:48902]

Fujita K; Yamauchi M; Matsui T; Titani K; Takahashi H; Kato T; Isomura G; Ando M; Nagata Y. 1998. Increase of glial fibrillary acidic protein fragments in the spinal cord of motor neuron degeneration mutant mouse. Brain Res 785(1):31-40. [PubMed: 9526038]  [MGI Ref ID J:51082]

Ghezzi P; Bernardini R; Giuffrida R; Bellomo M; Manzoni C; Comoletti D ; Di Santo E ; Benigni F ; Mennini T. 1998. Tumor necrosis factor is increased in the spinal cord of an animal model of motor neuron degeneration. Eur Cytokine Netw 9(2):139-44. [PubMed: 9681389]  [MGI Ref ID J:48610]

Griffin JL; Muller D; Woograsingh R; Jowatt V; Hindmarsh A; Nicholson JK; Martin JE. 2002. Vitamin E deficiency and metabolic deficits in neuronal ceroid lipofuscinosis described by bioinformatics. Physiol Genomics 11(3):195-203. [PubMed: 12388797]  [MGI Ref ID J:81309]

Guarneri R; Russo D; Cascio C; D'Agostino S; Galizzi G; Bigini P; Mennini T; Guarneri P. 2004. Retinal oxidation, apoptosis and age- and sex-differences in the mnd mutant mouse, a model of neuronal ceroid lipofuscinosis. Brain Res 1014(1-2):209-20. [PubMed: 15213005]  [MGI Ref ID J:90947]

Hawes NL; Smith RS; Chang B; Davisson M; Heckenlively JR; John SW. 1999. Mouse fundus photography and angiography: a catalogue of normal and mutant phenotypes. Mol Vis 5:22. [PubMed: 10493779]  [MGI Ref ID J:59481]

Holmes FE; Haynes LW. 1996. Superactivation of transglutaminase type 2 without change in enzyme level occurs during progressive neurodegeneration in the mnd mouse mutant. Neurosci Lett 213(3):185-8. [PubMed: 8873145]  [MGI Ref ID J:35599]

Li J; Nixon R; Messer A; Berman S; Bursztajn S. 1998. Altered gene expression for calpain/calpastatin system in motor neuron degeneration (Mnd) mutant mouse brain and spinal cord. Brain Res Mol Brain Res 53(1-2):174-86. [PubMed: 9473662]  [MGI Ref ID J:46702]

Mazurkiewicz JE. 1991. Ubiquitin deposits are present in spinal motor neurons in all stages of the disease in the motor neuron degeneration (Mnd) mutant of the mouse. Neurosci Lett 128(2):182-6. [PubMed: 1658691]  [MGI Ref ID J:624]

Mazurkiewicz JE; Callahan LM; Swash M; Martin JE; Messer A. 1993. Cytoplasmic inclusions in spinal neurons of the motor neuron degeneration (Mnd) mouse. I. Light microscopic analysis. J Neurol Sci 116(1):59-66. [PubMed: 8389815]  [MGI Ref ID J:4750]

Mennini T; Bastone A; Crespi D; Comoletti D; Manzoni C. 1998. Spinal cord GLT-1 glutamate transporter and blood glutamic acid alterations in motor neuron degeneration (Mnd) mice. J Neurol Sci 157(1):31-6. [PubMed: 9600674]  [MGI Ref ID J:47141]

Mennini T; Bigini P; Cagnotto A; Carvelli L; Di Nunno P; Fumagalli E; Tortarolo M; Buurman WA; Ghezzi P; Bendotti C. 2004. Glial activation and TNFR-I upregulation precedes motor dysfunction in the spinal cord of mnd mice. Cytokine 25(3):127-35. [PubMed: 14698139]  [MGI Ref ID J:101859]

Mennini T; Bigini P; Ravizza T; Vezzani A; Calvaresi N; Tortarolo M; Bendotti C. 2002. Expression of glutamate receptor subtypes in the spinal cord of control and mnd mice, a model of motor neuron disorder. J Neurosci Res 70(4):553-60. [PubMed: 12404509]  [MGI Ref ID J:105145]

Mennini T; Cagnotto A; Carvelli L; Comoletti D; Manzoni C; Muzio V ; Rizzi M ; Vezzani A. 1999. Biochemical and pharmacological evidence of a functional role of AMPA receptors in motor neuron dysfunction in mnd mice. Eur J Neurosci 11(5):1705-10. [PubMed: 10215924]  [MGI Ref ID J:55254]

Messer A; Flaherty L. 1986. Autosomal dominance in a late-onset motor neuron disease in the mouse. J Neurogenet 3(6):345-55. [PubMed: 3783318]  [MGI Ref ID J:8492]

Messer A; Manley K; Plummer JA. 1999. An early-onset congenic strain of the motor neuron degeneration (mnd) mouse. Mol Genet Metab 66(4):393-7. [PubMed: 10191135]  [MGI Ref ID J:56219]

Messer A; Plummer J. 1993. Accumulating autofluorescent material as a marker for early changes in the spinal cord of the Mnd mouse. Neuromuscul Disord 3(2):129-34. [PubMed: 8358238]  [MGI Ref ID J:16252]

Messer A; Plummer J; MacMillen MC; Frankel WN. 1995. Genetics of primary and timing effects in the mnd mouse. Am J Med Genet 57(2):361-4. [PubMed: 7668363]  [MGI Ref ID J:25748]

Messer A; Plummer J; Maskin P; Coffin JM; Frankel WN. 1992. Mapping of the motor neuron degeneration (Mnd) gene, a mouse model of amyotrophic lateral sclerosis (ALS). Genomics 13(3):797-802. [PubMed: 1639406]  [MGI Ref ID J:1224]

Messer A; Plummer J; Wong V; Lavail MM. 1993. Retinal degeneration in motor neuron degeneration (mnd) mutant mice [letter] Exp Eye Res 57(5):637-41. [PubMed: 8282051]  [MGI Ref ID J:19328]

Oh C; Murray B; Bhattacharya N; Holland D; Tatton WG. 1994. (-)-Deprenyl alters the survival of adult murine facial motoneurons after axotomy: increases in vulnerable C57BL strain but decreases in motor neuron degeneration mutants. J Neurosci Res 38(1):64-74. [PubMed: 8057392]  [MGI Ref ID J:18052]

Pardo CA; Rabin BA; Palmer DN; Price DL. 1994. Accumulation of the adenosine triphosphate synthase subunit C in the mnd mutant mouse. A model for neuronal ceroid lipofuscinosis. Am J Pathol 144(4):829-35. [PubMed: 8160780]  [MGI Ref ID J:17600]

Plummer J; Peterson A; Messer A. 1995. Accelerated and widespread neuronal loss occurs in motor neuron degeneration (mnd) mice expressing a neurofilament-disrupting transgene. Mol Cell Neurosci 6(6):532-43. [PubMed: 8742270]  [MGI Ref ID J:31812]

Porter JC; Messer A; Peterson A. 1997. The motor neuron degeneration (mnd) gene acts intrinsically in motor neurons and peripheral fibroblasts. Mol Cell Neurosci 9(3):185-93. [PubMed: 9245501]  [MGI Ref ID J:42419]

Ranta S; Zhang Y; Ross B; Lonka L; Takkunen E; Messer A; Sharp J; Wheeler R; Kusumi K; Mole S; Liu W; Soares MB; Bonaldo MF; Hirvasniemi A; de la Chapelle A; Gilliam TC; Lehesjoki AE. 1999. The neuronal ceroid lipofuscinoses in human EPMR and mnd mutant mice are associated with mutations in CLN8. Nat Genet 23(2):233-6. [PubMed: 10508524]  [MGI Ref ID J:57766]

Seigel GM; Wagner J; Wronska A; Campbell L; Ju W; Zhong N. 2005. Progression of early postnatal retinal pathology in a mouse model of neuronal ceroid lipofuscinosis. Eye 19(12):1306-12. [PubMed: 15565184]  [MGI Ref ID J:116862]

Vance JE; Stone SJ; Faust JR. 1997. Abnormalities in mitochondria-associated membranes and phospholipid biosynthetic enzymes in the mnd/mnd mouse model of neuronal ceroid lipofuscinosis. Biochim Biophys Acta 1344(3):286-99. [PubMed: 9059519]  [MGI Ref ID J:39062]

Wendt KD; Lei B; Schachtman TR; Tullis GE; Ibe ME; Katz ML. 2005. Behavioral assessment in mouse models of neuronal ceroid lipofuscinosis using a light-cued T-maze. Behav Brain Res 161(2):175-82. [PubMed: 15885820]  [MGI Ref ID J:98844]

Health & husbandry

Health & Colony Maintenance Information

Currently there no information available for this strain. This may be due to the supply level of this strain.

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Supply Details

Standard Supply

Repository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information.

Supply Notes

Cryorecovery - Standard. The recovery process begins when a signed agreement form is returned to the Customer Service Department after order placement. Although results vary by strain, at least two males and two females (two pairs) will be provided, typically within 15 weeks of our receipt of the signed agreement form. If the first recovery attempt is unsuccessful or only one pair is recovered, a second recovery will be done, extending the delivery time to approximately 25 weeks. At least one member of each pair will be of known genotype and will carry the mutation if it is a mutant strain. Please note that pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Price represents a repository maintenance fee, which includes the cost of recovery of the strain from the cryopreservation resource and the periodic replacement of the frozen embryos used for recovery. Cryorecovery to establish a Dedicated Supply for greater quantities of mice. One to two pairs will be recovered to establish a Dedicated Supply of mice. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 or 1-207-288-5845. This strain is included in the Mouse Mutant Resource collection. Genomic DNA is available for this strain from the Mouse DNA Resource.

Control Information

	Control
	Heterozygote from the colony
Considerations for Choosing Controls
USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains.
International - Control Pricing Information for Genetically Engineered Mutant Strains.

General Terms and Conditions

See Terms of Use

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX^® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX^® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX^® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.

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