Strain Name:

B6.129P2-Ugt8atm1Pop/J

Stock Number:

004751

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Availability:

Cryopreserved - Ready for recovery

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 Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Specieslaboratory mouse
 
Donating Investigator Brian Popko,   University of Chicago

Description
Mice that are homozygous for the targeted mutation have a postnatal lethal phenotype and most do not survive past postnatal day 21 to 28. Surviving homozygotes do not live past 100 days of age. Homozygous female mice are fertile but unable to care for pups. Homozygous male mice are infertile. No gene product (mRNA) is detected by Northern blot analysis of brain tissue from homozygote animals. Mice that are homozygous for the mutation are smaller in size than wildtype and heterozygous littermates. Beginning at 12-14 days of age, homozygotes develop mild ataxia, head jerking movements, and tremors that become more noticeable by 16-20 days of age. The abnormal neurological phenotype is progressive; by 60 days of age many mutants exhibit complete hindlimb paralysis and difficulty breathing. Homozygotes do not synthesize galactolipid galactocerebroside, heterozygotes exhibit reduced levels. Although myelin synthesis and myelin sheath (compact myelin) formation is mostly unaltered in homozygotes, nerve conduction is abnormal in the spinal cord. Electrophysiological analysis of nerve function is consistent with impaired myelin sheath insulative capacity. Histological and electron microscopic analysis reveals vacuolation in the ventral spinal cord and myelin splitting in 24 day old mice. 43 day old mice exhibit more severe myelin splitting, vacuolation of the optic nerve and abnormal node and paranode structure. The electrophysiological and structural abnormalities observed in the CNS are not as severe in the PNS. Levels of peripheral leukocytes and cell numbers in the thymus and spleen are significantly reduced. Spleen, inguinal lymph nodes and Peyer's patches are atrophic. Heterozygotes are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. This mutant mouse strain may be useful in studies of neuroelectrophysiology, nerve myelination and lymphopoiesis in the bone marrow.

Development
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt exon 2, which encodes the N-terminal region of the enzyme. The construct was electroporated into 129P2/OlaHsd derived BK4 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts. The resulting chimeric male animals were crossed to C57BL/6J mice, and then backcrossed to the same for more than 10 generations.

Control Information

  Control
   Wild-type from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

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

Ugt8atm1Pop/Ugt8a+

        involves: 129P2/OlaHsd * C57BL/6
  • homeostasis/metabolism phenotype
  • abnormal lipid level
    • reduced levels of galactocerebroside and sulfatide at 16 days of age   (MGI Ref ID J:77226)

Ugt8atm1Pop/Ugt8atm1Pop

        involves: 129P2/OlaHsd * C57BL/6
  • mortality/aging
  • premature death
    • some mice died between 18-30 days of age while others survived past 90 d of age   (MGI Ref ID J:77226)
  • behavior/neurological phenotype
  • abnormal head movements
    • mice exhibited jerking movement at 12-14 days of age   (MGI Ref ID J:77226)
  • ataxia
    • mice displayed mild ataxia at 12-14 days of age   (MGI Ref ID J:77226)
  • hindlimb paralysis
    • abnormal splaying and dragging of hindlimbs with clenched paws; progressive loss of hindlimb function leading to loss of locomotor ability by 60 d of age   (MGI Ref ID J:77226)
  • tremors
    • onset between 16-20 days of age; apparent at rest, but more pronounced during movement   (MGI Ref ID J:77226)
  • growth/size/body phenotype
  • decreased body weight
    • mice weighed 33-66% less than heterozygous and wild-type littermates   (MGI Ref ID J:77226)
  • homeostasis/metabolism phenotype
  • abnormal lipid level
    • absence of galactocerebroside and sulfatide   (MGI Ref ID J:77226)
  • immune system phenotype
  • *normal* immune system phenotype
    • normal natural killer T cell development and function   (MGI Ref ID J:78426)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • normal myelin ultrastructure; no vacular degeneration observed in PNS myelin normal myelin ultrastructure; no vacuolar degeneration observed in PNS myelin   (MGI Ref ID J:78426)
    • abnormal myelination
      • compact myelin displayed at 24 d of age   (MGI Ref ID J:78426)
      • decrease in thickness of dorsal spinal white matter myelin   (MGI Ref ID J:78426)
      • 30% decrease in mean thickness of ventral spinal white matter myelin   (MGI Ref ID J:78426)
      • myelin splitting evident in mice 24 d of age, progression with age   (MGI Ref ID J:78426)
      • vacuolization evident in the ventral region of the spinal cord in mice 24 d of age, progression with age   (MGI Ref ID J:78426)
      • abnormal node and paranode formation   (MGI Ref ID J:78426)
    • abnormal nerve conduction
      • associated with increased distribution of potassium channel, extending through internodal region   (MGI Ref ID J:58935)
      • 50% reduction in compound action potential amplitude; 30-40% reduction in conductance velocity of sciatic nerve   (MGI Ref ID J:78426)

Ugt8atm1Pop/Ugt8atm1Pop

        involves: 129P2/OlaHsd
  • nervous system phenotype
  • abnormal Purkinje cell morphology
    • large numbers of axonal swellings on Purkinje cells   (MGI Ref ID J:107653)
    • loss of axoglial junctions   (MGI Ref ID J:107653)
    • accumulation of mitochondria in axonal swellings   (MGI Ref ID J:107653)
    • paranodal transverse septa are absent   (MGI Ref ID J:107653)
    • disorganized and misoriented microtubules   (MGI Ref ID J:107653)
View Research Applications

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

Developmental Biology Research
Neurodevelopmental Defects

Neurobiology Research
Ataxia (Movement) Defects
Metabolic Defects
Myelination Defects
Neurodevelopmental Defects
Neuromuscular Defects
Tremor Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Ugt8atm1Pop
Allele Name targeted mutation 1, Brian Popko
Allele Type Targeted (knock-out)
Common Name(s) CGTnull; Cgt-; Cgt0;
Strain of Origin129P2/OlaHsd
ES Cell Line NameBK4
ES Cell Line Strain129P2/OlaHsd
Gene Symbol and Name Ugt8a, UDP galactosyltransferase 8A
Chromosome 3
Gene Common Name(s) AI850488; AW455908; CGT; Cgt; UDP glucuronosyltransferase 8; UDP-galactose ceramide galactosyltransferase; UGT4; Ugt8; expressed sequence AI850488; expressed sequence AW455908; mCerGT;
Molecular Note Exon 2 was disrupted by the insertion of a neomycin selection cassette 219 base pairs downstream of the translational start codon. Northern blot analyses showed the exclusive presence of truncated transcript containing the neo transgene in homozgous mutant mice. [MGI Ref ID J:77226]

Genotyping

Genotyping Information

Genotyping Protocols

Ugt8atm1Pop, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Coetzee T; Fujita N; Dupree J; Shi R; Blight A; Suzuki K; Suzuki K; Popko B. 1996. Myelination in the absence of galactocerebroside and sulfatide: normal structure with abnormal function and regional instability. Cell 86(2):209-19. [PubMed: 8706126]  [MGI Ref ID J:77226]

Additional References

Ugt8atm1Pop related

Coetzee T; Dupree JL; Popko B. 1998. Demyelination and altered expression of myelin-associated glycoprotein isoforms in the central nervous system of galactolipid-deficient mice. J Neurosci Res 54(5):613-22. [PubMed: 9843152]  [MGI Ref ID J:113183]

Coetzee T; Suzuki K; Nave KA; Popko B. 1999. Myelination in the absence of galactolipids and proteolipid proteins. Mol Cell Neurosci 14(1):41-51. [PubMed: 10433816]  [MGI Ref ID J:57688]

Dupree JL; Coetzee T; Blight A; Suzuki K; Popko B. 1998. Myelin galactolipids are essential for proper node of Ranvier formation in the CNS. J Neurosci 18(5):1642-9. [PubMed: 9464989]  [MGI Ref ID J:78426]

Dupree JL; Girault JA; Popko B. 1999. Axo-glial interactions regulate the localization of axonal paranodal proteins. J Cell Biol 147(6):1145-52. [PubMed: 10601330]  [MGI Ref ID J:58935]

Dupree JL; Popko B. 1999. Genetic dissection of myelin galactolipid function. J Neurocytol 28(4-5):271-9. [PubMed: 10739570]  [MGI Ref ID J:61229]

Ezoe T; Vanier MT; Oya Y; Popko B; Tohyama J; Matsuda J; Suzuki K; Suzuki K. 2000. Biochemistry and neuropathology of mice doubly deficient in synthesis and degradation of galactosylceramide. J Neurosci Res 59(2):170-8. [PubMed: 10650875]  [MGI Ref ID J:113298]

Ezoe T; Vanier MT; Oya Y; Popko B; Tohyama J; Matsuda J; Suzuki K; Suzuki K. 2000. Twitcher mice with only a single active galactosylceramide synthase gene exhibit clearly detectable but therapeutically minor phenotypic improvements. J Neurosci Res 59(2):179-87. [PubMed: 10650876]  [MGI Ref ID J:113251]

Fewou SN; Fernandes A; Stockdale K; Francone VP; Dupree JL; Rosenbluth J; Pfeiffer SE; Bansal R. 2010. Myelin protein composition is altered in mice lacking either sulfated or both sulfated and non-sulfated galactolipids. J Neurochem 112(3):599-610. [PubMed: 19878436]  [MGI Ref ID J:156246]

Garcia-Fresco GP; Sousa AD; Pillai AM; Moy SS; Crawley JN; Tessarollo L; Dupree JL; Bhat MA. 2006. Disruption of axo-glial junctions causes cytoskeletal disorganization and degeneration of Purkinje neuron axons. Proc Natl Acad Sci U S A 103(13):5137-42. [PubMed: 16551741]  [MGI Ref ID J:107653]

Jahng A; Maricic I; Aguilera C; Cardell S; Halder RC; Kumar V. 2004. Prevention of autoimmunity by targeting a distinct, noninvariant CD1d-reactive T cell population reactive to sulfatide. J Exp Med 199(7):947-57. [PubMed: 15051763]  [MGI Ref ID J:121032]

Katayama Y; Battista M; Kao WM; Hidalgo A; Peired AJ; Thomas SA; Frenette PS. 2006. Signals from the sympathetic nervous system regulate hematopoietic stem cell egress from bone marrow. Cell 124(2):407-21. [PubMed: 16439213]  [MGI Ref ID J:115906]

Katayama Y; Frenette PS. 2003. Galactocerebrosides are required postnatally for stromal-dependent bone marrow lymphopoiesis. Immunity 18(6):789-800. [PubMed: 12818160]  [MGI Ref ID J:84041]

Kongmanas K; Xu H; Yaghoubian A; Franchini L; Panza L; Ronchetti F; Faull K; Tanphaichitr N. 2010. Quantification of seminolipid by LC-ESI-MS/MS-multiple reaction monitoring: compensatory levels in Cgt(+/) mice. J Lipid Res 51(12):3548-58. [PubMed: 20817833]  [MGI Ref ID J:167028]

Lullmann-Rauch R; Matzner U; Franken S; Hartmann D; Gieselmann V. 2001. Lysosomal sulfoglycolipid storage in the kidneys of mice deficient for arylsulfatase A (ASA) and of double-knockout mice deficient for ASA and galactosylceramide synthase. Histochem Cell Biol 116(2):161-9. [PubMed: 11685544]  [MGI Ref ID J:120809]

Marcus J; Dupree JL; Popko B. 2000. Effects of galactolipid elimination on oligodendrocyte development and myelination. Glia 30(4):319-28. [PubMed: 10797612]  [MGI Ref ID J:113081]

Marcus J; Dupree JL; Popko B. 2002. Myelin-associated glycoprotein and myelin galactolipids stabilize developing axo-glial interactions. J Cell Biol 156(3):567-77. [PubMed: 11827985]  [MGI Ref ID J:77227]

Poliak S; Gollan L; Salomon D; Berglund EO; Ohara R; Ranscht B; Peles E. 2001. Localization of Caspr2 in myelinated nerves depends on axon-glia interactions and the generation of barriers along the axon. J Neurosci 21(19):7568-75. [PubMed: 11567047]  [MGI Ref ID J:124251]

Saadat L; Dupree JL; Kilkus J; Han X; Traka M; Proia RL; Dawson G; Popko B. 2010. Absence of oligodendroglial glucosylceramide synthesis does not result in CNS myelin abnormalities or alter the dysmyelinating phenotype of CGT-deficient mice. Glia 58(4):391-8. [PubMed: 19705459]  [MGI Ref ID J:159345]

Schafer DP; Bansal R; Hedstrom KL; Pfeiffer SE; Rasband MN. 2004. Does paranode formation and maintenance require partitioning of neurofascin 155 into lipid rafts? J Neurosci 24(13):3176-85. [PubMed: 15056697]  [MGI Ref ID J:109788]

Stanic AK; De Silva AD; Park JJ; Sriram V; Ichikawa S; Hirabyashi Y; Hayakawa K; Van Kaer L; Brutkiewicz RR; Joyce S. 2003. Defective presentation of the CD1d1-restricted natural Va14Ja18 NKT lymphocyte antigen caused by beta-D-glucosylceramide synthase deficiency. Proc Natl Acad Sci U S A 100(4):1849-54. [PubMed: 12576547]  [MGI Ref ID J:81972]

Tadano-Aritomi K; Hikita T; Fujimoto H; Suzuki K; Motegi K; Ishizuka I. 2000. Kidney lipids in galactosylceramide synthase-deficient mice. Absence Of galactosylsulfatide and compensatory increase in more polar sulfoglycolipids J Lipid Res 41(8):1237-43. [PubMed: 10946011]  [MGI Ref ID J:64029]

Traka M; Dupree JL; Popko B; Karagogeos D. 2002. The neuronal adhesion protein TAG-1 is expressed by Schwann cells and oligodendrocytes and is localized to the juxtaparanodal region of myelinated fibers. J Neurosci 22(8):3016-24. [PubMed: 11943804]  [MGI Ref ID J:125653]

Traka M; Wollmann RL; Cerda SR; Dugas J; Barres BA; Popko B. 2008. Nur7 is a nonsense mutation in the mouse aspartoacylase gene that causes spongy degeneration of the CNS. J Neurosci 28(45):11537-49. [PubMed: 18987190]  [MGI Ref ID J:143201]

Zoller I; Bussow H; Gieselmann V; Eckhardt M. 2005. Oligodendrocyte-specific ceramide galactosyltransferase (CGT) expression phenotypically rescues CGT-deficient mice and demonstrates that CGT activity does not limit brain galactosylceramide level. Glia 52(3):190-8. [PubMed: 15968630]  [MGI Ref ID J:156151]

Health & husbandry

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.

Health & Colony Maintenance Information

Animal Health Reports

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

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice are bred as heterozygotes due to the homozygous postnatal lethal phenotype. Homozygous female mice are fertile but unable to care for pups. Homozygous male mice are infertile.

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* $2450.00
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 11 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* $3185.00
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 11 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
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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