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. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Species laboratory mouse Generation N2F4pN1 Generation Definitions   Donating Investigator James W Dennis,   Samuel Lunenfeld Research Institute

Description
No gene product (protein) is detected by Western blot analysis and enzyme activity is undetectable. Beta-galactosidase activity mimics endogenous gene expression patterns. Homozygotes exhibit abnormal increased leukocyte infiltration in kidney tissue, which is indicative of kidney autoimmune glomerulonephritis. Induced experimental autoimmune encephalomyelitis (EAE) and induced delayed-type hypersensitivity (DTH) responses are increased in homozygotes. Cultured splenocytes isolated from homozygotes produce 2 fold more IFN-gamma and 2 fold less IL4. Mutant mice exhibit delayed tumor progression when bred with oncomice (for example, when crossed to a polyomavirus middle T antigen expressing transgenic strain). Mice that are homozygous for the targeted mutation are viable, normal in size and do not display any gross physical or behavioral abnormalities. The Donating Investigator reports that homozygous females are not fertile. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, autoimmunity and antitumor immunity.

This strain was transferred from the collection of the Consortium for Functional Glycomics.

Development
A targeting vector containing neomycin resistance and beta-galactosidase genes was used to disrupt exon 1. The construct was electroporated into 129 derived R1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into recipient blastocysts. The resulting male chimeric animals were crossed to 129 female mice, and then backcrossed to C57BL/6 for 9 generations before arriving at The Jackson Laboratory.

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.

Mgat5^tm1Jwd/Mgat5^tm1Jwd

        involves: 129S1/Sv * 129X1/SvJ

• immune system phenotype
• abnormal inflammatory response
  • abnormal recruitment of leukocytes into inflamed tissue   (MGI Ref ID J:60960)
• abnormal leukocyte physiology
  • increased splenocyte proliferation after stimulation   (MGI Ref ID J:94864)
• • abnormal T cell physiology
    • T cells hypersensitive to T cell receptor agonists   (MGI Ref ID J:60960)
• decreased interleukin-2 secretion
  • Il2 production is reduced   (MGI Ref ID J:94864)
• decreased interleukin-4 secretion
  • Il4 production is reduced about 2 fold per cell   (MGI Ref ID J:94864)
• increased interleukin-10 secretion
  • production is increased   (MGI Ref ID J:94864)
• increased tumor necrosis factor secretion
  • TNF-alpha production is increased more than 2-fold   (MGI Ref ID J:94864)
• tumorigenesis
• decreased metastatic potential
  • lung cancer metastasis about 50% of controls and never causes cardiac hypertrophy   (MGI Ref ID J:60960)
• decreased tumor growth/size
  • tumor growth much slower (3.4g at 28-30 weeks as opposed to 15g in controls)   (MGI Ref ID J:60960)
• increased tumor latency
  • 50% reduction in the incidence of mammary tumors at 24 weeks of age rather than at 16 weeks as in controls   (MGI Ref ID J:60960)
  • male tumor development at 10-13 months of age rather than at 6-9 months   (MGI Ref ID J:60960)
  • tumor foci development is normal   (MGI Ref ID J:60960)
• renal/urinary system phenotype
• abnormal renal glomerulus morphology
  • age related reduction in cellularity of the kidney glomerulus   (MGI Ref ID J:60960)
• behavior/neurological phenotype
• abnormal maternal nurturing
  • deficiencies in nurturing behavior   (MGI Ref ID J:60960)
• homeostasis/metabolism phenotype
• abnormal homeostasis
  • mice exhibit lack N-linked beta1,6-branched glycans   (MGI Ref ID J:188930)
  • however, mice exhibit normal levels of O-man-linked beta1,6-branched glycans   (MGI Ref ID J:188930)

View Research Applications

Research Applications

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

Cell Biology Research
Protein Processing

Immunology, Inflammation and Autoimmunity Research
Autoimmunity

Genes & Alleles

Gene & Allele Information provided by MGI

Allele Symbol		Mgat5tm1Jwd
Allele Name		targeted mutation 1, James W Dennis
Allele Type		Targeted (Reporter)
Common Name(s)		GnTV-; Mgat5-;
Mutation Made By		Peter Sobieszczuk,   Consortium for Functional Glycomics,TSRI
Strain of Origin		(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
ES Cell Line Name		R1
ES Cell Line Strain		(129X1/SvJ x 129S1/Sv)F1-Kitl<+>
Gene Symbol and Name		Mgat5, mannoside acetylglucosaminyltransferase 5
Chromosome		1
Gene Common Name(s)		4930471A21Rik; 5330407H02Rik; AI480971; GNT-V; GNT-VA; GlcNAc-TV; RIKEN cDNA 4930471A21 gene; RIKEN cDNA 5330407H02 gene; beta1,6N-acetylglucosaminyltransferase V; expressed sequence AI480971;
Molecular Note		A LacZ and neomycin resistance cassette replaced part of exon 1. [MGI Ref ID J:60960]

Genotyping

Genotyping Information

Genotyping Protocols

Mgat5^tm1Jwd, Standard PCR

Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Granovsky M; Fata J; Pawling J; Muller WJ; Khokha R; Dennis JW. 2000. Suppression of tumor growth and metastasis in Mgat5-deficient mice. Nat Med 6(3):306-12. [PubMed: 10700233]  [MGI Ref ID J:60960]

Additional References

Mgat5^tm1Jwd related

Bahaie NS; Kang BN; Frenzel EM; Hosseinkhani MR; Ge XN; Greenberg Y; Ha SG; Demetriou M; Rao SP; Sriramarao P. 2011. N-Glycans differentially regulate eosinophil and neutrophil recruitment during allergic airway inflammation. J Biol Chem 286(44):38231-41. [PubMed: 21911487]  [MGI Ref ID J:178166]

Demetriou M; Granovsky M; Quaggin S; Dennis JW. 2001. Negative regulation of T-cell activation and autoimmunity by Mgat5 N-glycosylation. Nature 409(6821):733-9. [PubMed: 11217864]  [MGI Ref ID J:111264]

Guo HB; Johnson H; Randolph M; Nagy T; Blalock R; Pierce M. 2010. Specific posttranslational modification regulates early events in mammary carcinoma formation. Proc Natl Acad Sci U S A 107(49):21116-21. [PubMed: 21078982]  [MGI Ref ID J:167163]

Guo HB; Lee I; Bryan BT; Pierce M. 2005. Deletion of mouse embryo fibroblast N-acetylglucosaminyltransferase V stimulates alpha5beta1 integrin expression mediated by the protein kinase C signaling pathway. J Biol Chem 280(9):8332-42. [PubMed: 15615721]  [MGI Ref ID J:97247]

Guo HB; Lee I; Kamar M; Pierce M. 2003. N-acetylglucosaminyltransferase V expression levels regulate cadherin-associated homotypic cell-cell adhesion and intracellular signaling pathways. J Biol Chem 278(52):52412-24. [PubMed: 14561752]  [MGI Ref ID J:87101]

Guo HB; Nairn A; Harris K; Randolph M; Alvarez-Manilla G; Moremen K; Pierce M. 2008. Loss of expression of N-acetylglucosaminyltransferase Va results in altered gene expression of glycosyltransferases and galectins. FEBS Lett 582(4):527-35. [PubMed: 18230362]  [MGI Ref ID J:131841]

Lee JK; Matthews RT; Lim JM; Swanier K; Wells L; Pierce JM. 2012. Developmental expression of the neuron-specific N-acetylglucosaminyltransferase Vb (GnT-Vb/IX) and identification of its in vivo glycan products in comparison with those of its paralog, GnT-V. J Biol Chem 287(34):28526-36. [PubMed: 22715095]  [MGI Ref ID J:188930]

Lee SU; Grigorian A; Pawling J; Chen IJ; Gao G; Mozaffar T; McKerlie C; Demetriou M. 2007. N-glycan processing deficiency promotes spontaneous inflammatory demyelination and neurodegeneration. J Biol Chem 282(46):33725-34. [PubMed: 17855338]  [MGI Ref ID J:128384]

Markowska AI; Liu FT; Panjwani N. 2010. Galectin-3 is an important mediator of VEGF- and bFGF-mediated angiogenic response. J Exp Med 207(9):1981-93. [PubMed: 20713592]  [MGI Ref ID J:165731]

Morgan R; Gao G; Pawling J; Dennis JW; Demetriou M; Li B. 2004. N-acetylglucosaminyltransferase v (Mgat5)-mediated N-glycosylation negatively regulates Th1 cytokine production by T cells. J Immunol 173(12):7200-8. [PubMed: 15585841]  [MGI Ref ID J:94864]

Ohtsubo K; Takamatsu S; Minowa MT; Yoshida A; Takeuchi M; Marth JD. 2005. Dietary and genetic control of glucose transporter 2 glycosylation promotes insulin secretion in suppressing diabetes. Cell 123(7):1307-21. [PubMed: 16377570]  [MGI Ref ID J:117542]

Partridge EA; Le Roy C; Di Guglielmo GM; Pawling J; Cheung P; Granovsky M; Nabi IR; Wrana JL; Dennis JW. 2004. Regulation of cytokine receptors by Golgi N-glycan processing and endocytosis. Science 306(5693):120-4. [PubMed: 15459394]  [MGI Ref ID J:93100]

Soleimani L; Roder JC; Dennis JW; Lipina T. 2008. Beta N-acetylglucosaminyltransferase V (Mgat5) deficiency reduces the depression-like phenotype in mice. Genes Brain Behav 7(3):334-43. [PubMed: 17883406]  [MGI Ref ID J:147477]

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 & Husbandry	When maintaining a live colony, these mice can be bred as heterozygous females and homozygous males. Homozygous females are infertile.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls

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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Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

See Terms of Use tab for General Terms and Conditions

The Jackson Laboratory's Genotype Promise

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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