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Type Mutant Stock; Spontaneous Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Generation N28 F1
Generation DefinitionsAppearance
black
Related Genotype: a/aDescription
Mice homozygous for the wasted spontaneous mutation (Eef1a2wst) can be recognized at 20 days of age by tremor and uncoordinated body movements. Homozygous mutant mice develop progressive paralysis and do not survive beyond 30 days. They have marked lymphoid hypoplasia in the spleen, thymus, lymph nodes, and peripheral blood. Wasted mice have a severely reduced number of IgA plasma cells in the entire large and small intestines, but the number of such cells in the spleen and the level of serum IgA are normal.Neuronal degeneration occurs in the brain and spinal cord. Spinal cord abnormalities are preceded by gliosis following along a rostrocaudal gradient. Thoracic/abdominal muscles exhibit a progressive denervation of muscle fibers, with progressive asynchronous retraction of motor nerve terminals. (Newbery HJ, et al. 2005)
Development
The wasted mutation arose spontaneously on the HRS/J background in 1972 and was subsequently maintained by breeding hosts of homozygous ovarian transplants to B6C3Fe-a/a F1 then intercrossing the heterozygous offspring. In 1987 heterozygotes at generation N28F1 were intercrossed to generate embryos for cryopreservation.
| Control | ||
|---|---|---|
| Untyped from the colony | ||
| Considerations for Choosing Controls | ||
Strains carrying a allele
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View Related Disease (OMIM) Terms
Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested. Skin/Hair/Eye Pigmentation, Variation In, 9; SHEP9 (ASIP)
View Mammalian Phenotype Terms
Mammalian Phenotype Terms provided by MGI
assigned by genotype
Eef1a2wst/Eef1a2wst
B6C3Fe a/a-Eef1a2wst/J
- mortality/aging
- premature death
- average age of death is 28 days (MGI Ref ID J:24753)
- behavior/neurological phenotype
- paraparesis
- increasing flacidity of the hind legs and an overall debilitated appearance follow the onset of tremor at 20 days of age (MGI Ref ID J:24753)
- tremors
- fine intention tremor over the entire body is visible by approximately 20 days of age (MGI Ref ID J:24753)
- nervous system phenotype
- Purkinje cell degeneration
- evident by 22 to 29 days of age (MGI Ref ID J:6766)
- demyelination
- at 22 to 29 days of age focal demyelination is found in the ventral columns of the spinal cord and in the cerebellar cortex (MGI Ref ID J:6766)
- immune system phenotype
- decreased plasma cell number
- although the intestinal villi are normal in size, there is a progressive decline in gut IgA plasma cells and no detectable IgA plasma cells in the gut lamina propria and submucosae by 27 days of age (MGI Ref ID J:7903)
- decreased spleen weight
- consistent with lymphoid hypoplasia the ratio of spleen weight to body weight is less than half that of normal (MGI Ref ID J:6766)
- decreased susceptibility to type IV hypersensitivity reaction
- less footpad inflammation than heterozygous controls in response to injected sheep red blood cells 4 days after priming (MGI Ref ID J:6766)
- decreased thymus weight
- consistent with lymphoid hypoplasia the ratio of thymic weight to body weight is much smaller than normal (MGI Ref ID J:6766)
- lymphoid hypoplasia
- by 28 days of age homozygotes have a threefold diminution in the number of circulating leukocytes, decreased ratios of spleen, thymus, and lymph nodes to body weight, few and small Peyer's patches, reduction in cellularity of the thymic cortex, and poorly developed follicles in the lymph nodes and splee (MGI Ref ID J:6766)
- the percentages of T and B cells is normal with the lymphoid hypoplasia not being restricted to a lymphocyte subpopulation (MGI Ref ID J:6766)
- small lymph nodes
- consistent with lymphoid hypoplasia the ratio of brachial lymph node weight to body weight is much smaller than normal (MGI Ref ID J:6766)
- cellular phenotype
- chromosomal instability
- bone marrow cells from 23 to 28 day old homozygotes shows fourfold greater incidence of chromosomal damage, such as chromatid breaks, gaps, and fragments, than is found in heterozygous littermate controls (MGI Ref ID J:6766)
- increased cellular sensitivity to gamma-irradiation
- 2 of 2 homozygotes exposed to 220R from a cesium irradiator then treated with colchicine have chromosomal damage in 80% of 30 metaphase cells from bone marrow cell suspensions while controls have only monor damage in 30% of the cells scored (MGI Ref ID J:6766)
- growth/size phenotype
- slow postnatal weight gain
- no weight increase after 20 days of age (MGI Ref ID J:6766)
- weight loss
- at 24 days of age there is a sudden onset emaciated appearance from the ribs caudally (MGI Ref ID J:24753)
- hematopoietic system phenotype
- decreased plasma cell number
- although the intestinal villi are normal in size, there is a progressive decline in gut IgA plasma cells and no detectable IgA plasma cells in the gut lamina propria and submucosae by 27 days of age (MGI Ref ID J:7903)
- decreased spleen weight
- consistent with lymphoid hypoplasia the ratio of spleen weight to body weight is less than half that of normal (MGI Ref ID J:6766)
- decreased thymus weight
- consistent with lymphoid hypoplasia the ratio of thymic weight to body weight is much smaller than normal (MGI Ref ID J:6766)
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Eef1a2wst/Eef1a2wst
involves: HRS/J
- muscle phenotype
- abnormal muscle morphology
- by 20 days of age there is a decline in muscle mass and by 27 days of age the ratio of muscle to body weight is 1.49 compared with 4.44 in heterozygotes (MGI Ref ID J:104855)
- nervous system phenotype
- abnormal endplate potential
- at 23 days of age 20% of neuromuscular junctions in transverse abdominus muscles show weak synaptic transmission with random failures (MGI Ref ID J:104855)
- evoked endplate potentials in flexor digitorum brevis muscles do not show weak synaptic transmission until 25 days of age so there is progressive rostrocaudal deterioration in synaptic transmission (MGI Ref ID J:104855)
- abnormal motor neuron morphology
- in addition to vacuolation, an abnormal accumulation of phosphorylated neurofilaments is found in the motor neurons of the anterior horn of the cervical spinal cord (MGI Ref ID J:104855)
- motor neuron degeneration (MGI Ref ID J:104855)
- abnormal muscle innervation
- there is a rostrocaudal progressive retraction of motor nerve terminals (MGI Ref ID J:104855)
- abnormal neuromuscular synapse morphology
- as early as 17 days of age a small population of motor endplates is found to have no overlying motor nerve terminal, and this progresses such that by 27 days of age approximately 42% of endplates have no overlying motor nerve terminal (MGI Ref ID J:104855)
- abnormal neurotransmitter uptake
- FM1-43 and TRITC alpha bungarotoxin staining shows diminished uptake in a majority of endplates of transversus abdominus muscles from 25 day old homozygotes (MGI Ref ID J:104855)
- abnormal spinal cord ventral horn morphology
- at 28 days of age, but not 24 days of age, vacuolation is found in the anterior horn cells, but not at the lumbar level of the spinal cord (MGI Ref ID J:104855)
- decreased neurotransmitter release
- diminished spontaneous miniature endplate potentials in transversus abdominus muscles at 25 days of age (MGI Ref ID J:104855)
- gliosis
- although there is no evidence even at 29 days of age of microgliosis by CD45 staining, strong foci of GFAP staining in the anterior horn shows cervical, and to a lesser degree thoracic and lumbar, gliosis as early as 19 days of age (MGI Ref ID J:104855)
- behavior/neurological phenotype
- impaired coordination
- from 21 days of age on homozygotes are progressively less able to stay on a rotarod for as long as normal littermate controls (MGI Ref ID J:104855)
Eef1a2wst/Eef1a2wst
Background Not Specified
- hematopoietic system phenotype
- thymus atrophy
- at 27 days of age the thymus is less than half the normal diameter, has a substantial increase in the number of apoptotic cells, but near-normal proportions of thymocyte subpopulations (MGI Ref ID J:50410)
- immune system phenotype
- thymus atrophy
- at 27 days of age the thymus is less than half the normal diameter, has a substantial increase in the number of apoptotic cells, but near-normal proportions of thymocyte subpopulations (MGI Ref ID J:50410)
View Research Applications
Research Applications
This mouse can be used to support research in many areas including:Eef1a2wst related
Immunology, Inflammation and Autoimmunity Research
Immunodeficiency Associated with Other Defects
Internal/Organ Research
Lymphoid Tissue Defects
Spleen Defects
Neurobiology Research
Neuromuscular Defects
| Allele Symbol | Eef1a2wst | ||
|---|---|---|---|
| Allele Name | wasted | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | wst; | ||
| Strain of Origin | HRS/J | ||
| Gene Symbol and Name | Eef1a2, eukaryotic translation elongation factor 1 alpha 2 | ||
| Chromosome | 2 | ||
| Gene Common Name(s) | EEF1AL; EF-1-alpha-2; EF1A; Eef1a; HS1; Ps10; RATPS10; S1; STN; STNL; wasted; wst; | ||
| General Note | The enzymatic specific activity of ADA (which takes into account the reduced tissue weights of wasted mice) is increased in the spleen and cerebellum but decreased in the thymus of these mutants (J:12932). Wasted mutant mice have marked lymphoid hypoplasia in the spleen, thymus, lymph nodes, and peripheral blood. Wasted mice show some similarities to human ataxia telangiectasia (AT; MIM 208900; human gene, ATM; mouse gene, Atm) (J:6766), but there are also numerous differences. But the mutant mice lack the increased sensitivity of spleen cells to killing by ultraviolet radiation (J:20567), the increased sensitivity of cultured fibroblasts to killing by X or gamma radiation (J:8348, J:13960), and the increased post-irradiation inhibition of DNA synthesis (J:7561) characteristic of AT. In addition, the immunological defects of wasted mice differ considerably from those in human AT (J:8288). Wasted mice have a severely reduced number of IgA plasma cells in the entire large and small intestine, but the levelof such cells in spleen and the level of serum IgA are normal (J:7903). The mutants also show an extensive cytokine imbalance of many immunologically relevant gene products (IL5, IL1, IL2, IFNG, and TGFB1) which may trigger the wasted pathogenesis (J:19431). The overlapping similarities between AT and wasted, however, have suggested the possibility that Eef1a2 and Atm may be involved in a common pathway, such as a signal-transduction pathway that regulates protein synthesis (J:48050). In fact Eef1a2ws mice show abnormal expression of the proliferating cellular nuclear antigen (PCNA) in the thymus (J:37955). | ||
| Molecular Note | The mutation is a 15.8kb deletion that removes the promoter region and first noncoding exon of the gene. [MGI Ref ID J:47466] | ||
| Allele Symbol | a | ||
| Allele Name | nonagouti | ||
| Allele Type | Spontaneous | ||
| Strain of Origin | old mutant of the mouse fancy | ||
| Gene Symbol and Name | a, nonagouti | ||
| Chromosome | 2 | ||
| Gene Common Name(s) | AGSW; AGTI; AGTIL; ASP; As; SHEP9; agouti; agouti signal protein; agouti suppressor; | ||
| Molecular Note | Characterization of this allele shows an insertion of DNA comprised of a 5.5kb virus-like element, VL30, into the first intron of the agouti gene. The VL30 element itself contains an additional 5.5 kb sequence, flanked by 526 bp of direct repeats. The host integration site is the same as for at-2Gso and Aw-38J and includes a duplication of four nucleotides of host DNA and a deletion of 2 bp from the end of each repeat. Northern analysis of mRNA from skin of homozygotes shows a smaller agouti message and levels 8 fold lower than found in wild-type. [MGI Ref ID J:16984] [MGI Ref ID J:24934] | ||
Genotyping Protocols
Eef1a2wst, Separated PCR
Helpful Links
Genotyping resources and troubleshooting
Kaiserlian D; Delacroix D; Bach JF. 1985. The wasted mutant mouse. I. An animal model of secretory IgA deficiency with normal serum IgA. J Immunol 135(2):1126-31. [PubMed: 3874230] [MGI Ref ID J:7903]
Pan J; Ruest LB; Xu S; Wang E. 2004. Immuno-characterization of the switch of peptide elongation factors eEF1A-1/EF-1alpha and eEF1A-2/S1 in the central nervous system during mouse development. Brain Res Dev Brain Res 149(1):1-8. [PubMed: 15013623] [MGI Ref ID J:88820]
Shultz LD; Sweet HO; Davisson MT; Coman DR. 1982. 'Wasted', a new mutant of the mouse with abnormalities characteristic to ataxia telangiectasia. Nature 297(5865):402-4. [PubMed: 7078649] [MGI Ref ID J:6766]
Eef1a2wst relateda relatedAbbott CM; Skidmore CJ; Searle AG; Peters J. 1986. Deficiency of adenosine deaminase in the wasted mouse. Proc Natl Acad Sci U S A 83(3):693-5. [PubMed: 3456164] [MGI Ref ID J:8181]
Chambers DM; Peters J; Abbott CM. 1998. The lethal mutation of the mouse wasted (wst) is a deletion that abolishes expression of a tissue-specific isoform of translation elongation factor 1alpha, encoded by the Eef1a2 gene. Proc Natl Acad Sci U S A 95(8):4463-8. [PubMed: 9539760] [MGI Ref ID J:47466]
Geiger JD; Nagy JI. 1986. Lack of adenosine deaminase deficiency in the mutant mouse wasted. FEBS Lett 208(2):431-4. [PubMed: 3780980] [MGI Ref ID J:12932]
Griffiths LA; Doig J; Churchhouse AM; Davies FC; Squires CE; Newbery HJ; Abbott CM. 2012. Haploinsufficiency for translation elongation factor eEF1A2 in aged mouse muscle and neurons is compatible with normal function. PLoS One 7(7):e41917. [PubMed: 22848658] [MGI Ref ID J:189690]
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Inoue T; Aikawa K; Tezuka H; Kada T; Shultz LD. 1986. Effect of DNA-damaging agents on isolated spleen cells and lung fibroblasts from the mouse mutant wasted, a putative animal model for ataxia-telangiectasia. Cancer Res 46(8):3979-82. [PubMed: 2425937] [MGI Ref ID J:8348]
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Martin NM; Houston PA; Patterson M; Sajedi A; Carmignac DF; Ghatei MA; Bloom SR; Small CJ. 2006. Abnormalities of the somatotrophic axis in the obese agouti mouse. Int J Obes (Lond) 30(3):430-8. [PubMed: 16172617] [MGI Ref ID J:151302]
Martinez HG; Quinones MP; Jimenez F; Estrada CA; Clark K; Muscogiuri G; Sorice G; Musi N; Reddick RL; Ahuja SS. 2011. Critical role of chemokine (C-C motif) receptor 2 (CCR2) in the KKAy + Apoe -/- mouse model of the metabolic syndrome. Diabetologia 54(10):2660-8. [PubMed: 21779871] [MGI Ref ID J:177084]
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Miller MW; Duhl DM; Vrieling H; Cordes SP; Ollmann MM; Winkes BM; Barsh GS. 1993. Cloning of the mouse agouti gene predicts a secreted protein ubiquitously expressed in mice carrying the lethal yellow mutation. Genes Dev 7(3):454-67. [PubMed: 8449404] [MGI Ref ID J:4186]
Miyazaki M; Sampath H; Liu X; Flowers MT; Chu K; Dobrzyn A; Ntambi JM. 2009. Stearoyl-CoA desaturase-1 deficiency attenuates obesity and insulin resistance in leptin-resistant obese mice. Biochem Biophys Res Commun 380(4):818-22. [PubMed: 19338759] [MGI Ref ID J:147343]
Monroe DG; Wipf LP; Diggins MR; Matthees DP; Granholm NH. 1998. Agouti-related maturation and tissue distribution of alpha-Melanocyte Stimulating Hormone in wild-type (AwJ/AwJ) and mutant (Ay/a,a/a) mice. Pigment Cell Res 11(5):310-3. [PubMed: 9877102] [MGI Ref ID J:52183]
Moore KJ; Swing DA; Copeland NG; Jenkins NA. 1990. Interaction of the murine dilute suppressor gene (dsu) with fourteen coat color mutations [published erratum appears in Genetics 1990 Sep;126(1):285] Genetics 125(2):421-30. [PubMed: 2379821] [MGI Ref ID J:29467]
Moyer FH. 1966. Genetic variations in the fine structure and ontogeny of mouse melanin granules. Am Zool 6(1):43-66. [PubMed: 5902512] [MGI Ref ID J:5001]
Novak EK; Wieland F; Jahreis GP; Swank RT. 1980. Altered secretion of kidney lysosomal enzymes in the mouse pigment mutants ruby-eye, ruby-eye-2-J, and maroon. Biochem Genet 18(5-6):549-61. [PubMed: 6776948] [MGI Ref ID J:6422]
Nuotio-Antar AM; Hachey DL; Hasty AH. 2007. Carbenoxolone treatment attenuates symptoms of metabolic syndrome and atherogenesis in obese, hyperlipidemic mice. Am J Physiol Endocrinol Metab 293(6):E1517-28. [PubMed: 17878220] [MGI Ref ID J:145108]
Pettitt SJ; Liang Q; Rairdan XY; Moran JL; Prosser HM; Beier DR; Lloyd KC; Bradley A; Skarnes WC. 2009. Agouti C57BL/6N embryonic stem cells for mouse genetic resources. Nat Methods :. [PubMed: 19525957] [MGI Ref ID J:149352]
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Rice RH; Bradshaw KM; Durbin-Johnson BP; Rocke DM; Eigenheer RA; Phinney BS; Sundberg JP. 2012. Differentiating inbred mouse strains from each other and those with single gene mutations using hair proteomics. PLoS One 7(12):e51956. [PubMed: 23251662] [MGI Ref ID J:195664]
Rosenfeld CS; Sieli PT; Warzak DA; Ellersieck MR; Pennington KA; Roberts RM. 2013. Maternal exposure to bisphenol A and genistein has minimal effect on A(vy)/a offspring coat color but favors birth of agouti over nonagouti mice. Proc Natl Acad Sci U S A 110(2):537-42. [PubMed: 23267115] [MGI Ref ID J:193279]
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Animal Health Reports
Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.
| Pricing for USA, Canada and Mexico shipping destinations |
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Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $3175.00 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 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 |
|
Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $4127.50 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).
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Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.
| Control | ||
|---|---|---|
| Untyped from the colony | ||
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
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