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| Mgat5 (mannoside acetylglucosaminyltransferase 5) deficient mice exhibit increased responses to induced immune challenges and delayed tumor progression when bred with oncomice. This mutant mouse strain may be useful in studies of glycosidic molecular interactions and function, autoimmunity and antitumor immunity. | |||||||||||||||
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 Donating Investigator James 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 | ||
|---|---|---|
| Wild-type from the colony | ||
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
View Mammalian Phenotype Terms
Mammalian Phenotype Terms
assigned by genotype
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Mgat5tm1Jwd/Mgat5tm1Jwd
involves: 129S1/Sv * 129X1/SvJ
- immune system phenotype
- abnormal inflammatory response (MGI Ref ID J:60960)
- abnormal recruitment of leukocytes into inflamed tissue
- abnormal leukocyte physiology (MGI Ref ID J:94864)
- increased splenocyte proliferation after stimulation
- abnormal T cell physiology (MGI Ref ID J:60960)
- T cells hypersensitive to T cell receptor agonists
- decreased interleukin-2 secretion (MGI Ref ID J:94864)
- Il2 production is reduced
- decreased interleukin-4 secretion (MGI Ref ID J:94864)
- Il4 production is reduced about 2 fold per cell
- increased interleukin-10 secretion (MGI Ref ID J:94864)
- production is increased
- increased tumor necrosis factor secretion (MGI Ref ID J:94864)
- TNF-alpha production is increased more than 2-fold
- tumorigenesis
- decreased metastatic potential (MGI Ref ID J:60960)
- lung cancer metastasis about 50% of controls and never causes cardiac hypertrophy
- decreased tumor growth/size (MGI Ref ID J:60960)
- tumor growth much slower (3.4g at 28-30 weeks as opposed to 15g in controls)
- decreased tumor incidence (MGI Ref ID J:60960)
- 50% reduction in the incidence of mammary tumors at 24 weeks of age rather than at 16 weeks as in controls
- male tumor development at 10-13 months of age rather than at 6-9 months
- tumor foci development is normal
- renal/urinary system phenotype
- abnormal renal glomerulus morphology (MGI Ref ID J:60960)
- age related reduction in cellularity of the kidney glomerulus
- behavior/neurological phenotype
- abnormal maternal nurturing (MGI Ref ID J:60960)
- deficiencies in nurturing behavior
View Research Applications
Research Applications
This mouse can be used to support research in many areas including:
Cell Biology Research
Protein Processing
Immunology and Inflammation Research
Autoimmunity
| Allele Symbol | Mgat5tm1Jwd | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, James W Dennis | ||
| Allele Type | Targeted (Reporter) | ||
| Common Name(s) | 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 Protocols
Mgat5tm1Jwd, Standard PCR
Helpful Links
Genotyping resources and troubleshooting
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]
Mgat5tm1Jwd relatedDemetriou 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; 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 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]
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]
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 for USA, Canada and Mexico shipping destinations |
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Animals Provided
Price (US dollars $) Cryorecovery Fee $1900.00 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.
| Pricing for International shipping destinations |
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Animals Provided
Price (US dollars $) Cryorecovery Fee $2470.00 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 for further information. |
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| Supply Notes |
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| Control | ||
|---|---|---|
| Wild-type from the colony | ||
| 000664 C57BL/6J | ||
| 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. | ||
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