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- Description
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- Genes & alleles
- Genotyping
- Health & husbandry
- References
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Description
Strain Information
Type Congenic; Mutant Strain; Additional information on Genetically Engineered Mutant Mice. Species laboratory mouse Background Strain C57BL/6J Donor Strain Fancier H2 Haplotype b Generation F88 (21-JAN-08) Appearance
yellow, affected
Related Genotype: Ay/a
black, unaffected
Related Genotype: a/aDescription
Mice homozygous for the yellow spontaneous mutation (Ay) die before implantation or shortly thereafter. The time of death and type of abnormality is, in part, determined by the genetic background on which the mutation is placed. Hair pigment in heterozygous mice is yellow, but eyes are black. Heterozygotes usually become obese and infertile after the first few months. Increased adipose tissue mass is due to fat-cell hypertrophy. It has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine levels. Insulin resistance and hyperglycemia follow development of hyperinsulinemia in early adulthood, although the degree is less severe than on the KK/UpJ genetic background (Stock No. 002468). Heterozygotes are also more susceptible to several kinds of tumors than normal mice, and their spleen cells cause a significantly lower graft vs. host reaction. The level of malic enzyme in the liver is elevated.
Control Information
| Control | ||
|---|---|---|
| a/a from the colony | ||
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying Ay allele
005505 B6.Cg-Ay Slc7a11sut/LmLlp 002468 KK.Cg-Ay/J View Strains carrying Ay (2 strains)
Additional Web Information
Congenic Nomenclature
Genetic Quality Control Annual Report
Phenotype
Phenotype Information
Diabetes Mellitus, Noninsulin-Dependent; NIDDM - Models with phenotypic similarity to human disease where etiologies are distinct.2
2 Human genes are associated with this disease. Orthologs of those genes do not appear in the mouse genotype(s).
assigned by genotype
Ay/A
involves: C57BL/6
- adipose tissue phenotype
- abnormal gonadal fat pad morphology (MGI Ref ID J:131039)
- female mice have almost a 7-fold gain in weight of fat pad
- abnormal inguinal fat pad morphology (MGI Ref ID J:131039)
- female mice have a greater than 6-fold gain in weight of fat pad
- abnormal retroperitoneal fat pad morphology (MGI Ref ID J:131039)
- female mice have almost a 6-fold gain in weight of fat pad
- increased brown adipose tissue amount (MGI Ref ID J:131039)
- female mice have a 6-fold gain in weight of BAT compared to littermate controls
- increased percent body fat (MGI Ref ID J:131039)
- female mice have almost a 4-fold gain in percentage of body fat compared to littermate controls
- male mice have almost a 1.8-fold gain in percentage of body fat compared to littermate controls
- behavior/neurological phenotype
- hypoactivity (MGI Ref ID J:131039)
- the locomotor activity of mice is about half that of wild-type mice
- increased eating behavior (MGI Ref ID J:131039)
- 18 week old mice eat about 1.4 times more food during a 7 day period compared to wild-type controls
- growth/size phenotype
- increased body length (MGI Ref ID J:131039)
- female but not male mice have a significant 5% increase in their body length
- increased weight gain (MGI Ref ID J:131039)
- mice gain weight at a greater rate than littermate controls starting at six weeks of age
- by 23 weeks of age, female mice have almost double the weight compared to their wild-type littermate controls
- homeostasis/metabolism phenotype
- increased circulating leptin level (MGI Ref ID J:131039)
- circulating levels of leptin are over 12-fold higher compared to littermate controls
- liver/biliary system phenotype
- increased liver weight (MGI Ref ID J:131039)
- female mice have almost a 2-fold gain in weight of the liver
- pigmentation phenotype
- yellow coat color (MGI Ref ID J:131039)
- mice have a yellow coat color
- skin/coat/nails phenotype
- yellow coat color (MGI Ref ID J:131039)
- mice have a yellow coat color
Ay/a
B6.Cg-Ay/J
- behavior/neurological phenotype
- abnormal food intake (MGI Ref ID J:102986)
- the stress of isolation, restraint, or ip injection inhibits feeding
- pigmentation phenotype
- abnormal hair follicle melanogenesis (MGI Ref ID J:1295)
- tyrosinase levels in hairbulb melanocytes ,as determined by 35S methionine incorporation and immunotitration, are reduced in comparison to a/a controls
- decreased tyrosinase suggests the production of predominantly phaeomelanin (yellow)
- skin/coat/nails phenotype
- abnormal hair follicle melanogenesis (MGI Ref ID J:1295)
- tyrosinase levels in hairbulb melanocytes ,as determined by 35S methionine incorporation and immunotitration, are reduced in comparison to a/a controls
- decreased tyrosinase suggests the production of predominantly phaeomelanin (yellow)
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Ay/a
involves: KK
- homeostasis/metabolism phenotype
- abnormal lipid homeostasis (MGI Ref ID J:26460)
- lipogenesis from acetate is elevated at 5 weeks of age, the enhanced activity is maintained until 16 weeks of age
- the acetate/glucose ratio is higher than control in young mice
- hyperglycemia (MGI Ref ID J:26460)
- blood glucose levels increase with age in both sexes
- marked hyperglycemia (400-500 mg/dl) develops by 16 weeks of age
- impaired glucose tolerance (MGI Ref ID J:26460)
- increased circulating insulin level (MGI Ref ID J:26460)
- markedly elevated plasma immunoreactive insulin (IRI) level increases with age
- increased urine glucose level (MGI Ref ID J:26460)
- present at all ages tested (5, 10, 16 weeks) and in both sexes
- insulin resistance (MGI Ref ID J:26460)
- insulin sensitivity is impaired at 10 weeks and lost by 16 weeks
- adipose tissue phenotype
- increased adipose tissue amount (MGI Ref ID J:26460)
- adipose tissue weight increases with age, reaching a maximum at 10 weeks of age
- growth/size phenotype
- increased weight gain (MGI Ref ID J:26460)
- greater body weight gain occurs in females as compared to black KK controls
- endocrine/exocrine gland phenotype
- abnormal islet of Langerhans morphology (MGI Ref ID J:26460)
- islets are hypertrophic in 10-16 week old mice
- central cavity formation with occasional red blood cells is observed in islets
- abnormal pancreatic beta cell morphology (MGI Ref ID J:26460)
- beta cells are degranulated
- degranulated islets are infiltrated with fine glycogen granules
- digestive/alimentary phenotype
- abnormal islet of Langerhans morphology (MGI Ref ID J:26460)
- islets are hypertrophic in 10-16 week old mice
- central cavity formation with occasional red blood cells is observed in islets
- abnormal pancreatic beta cell morphology (MGI Ref ID J:26460)
- beta cells are degranulated
- degranulated islets are infiltrated with fine glycogen granules
- renal/urinary system phenotype
- abnormal renal glomerular capsule (MGI Ref ID J:26460)
- basement membrane of BowmanÕs capsules is thickened
- abnormal renal glomerulus morphology (MGI Ref ID J:26460)
- some glomeruli exhibit an accumulation of eosinophilic material in the outer parts of the capillary
- abnormal mesangial cell (MGI Ref ID J:26460)
- mesangial matrix is thickened
- abnormal renal tubule morphology (MGI Ref ID J:26460)
- basement membrane of tubules is thickened
- hyaline materials or hyaline cast is present in tubules
- dilated renal tubules (MGI Ref ID J:26460)
- increased urine glucose level (MGI Ref ID J:26460)
- present at all ages tested (5, 10, 16 weeks) and in both sexes
This mouse can be used to support research in many areas including:
Ay relatedDiabetes and Obesity Research
Hyperglycemia
Hyperinsulinemia
Insulin Resistance
Type 2 Diabetes (NIDDM)
Dermatology Research
Color and White Spotting Defects
Diabetes and Obesity Research
Obesity With Diabetes
Endocrine Deficiency Research
Adipose Defects
Adrenal Cortex Defects
Immunology and Inflammation Research
Immunodeficiency Associated with Other Defects
Internal/Organ Research
Adipose Defects
Adrenal Cortex Defects
Reproductive Biology Research
Endocrine Deficiencies Affecting Gonads
Fertility Defects
Research Tools
Reproductive Biology Research
Genes & Alleles
Gene & Allele Information
| Allele Symbol | Ay | ||
|---|---|---|---|
| Allele Name | yellow | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | A(y); Ay; | ||
| 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; MGC126092; MGC126093; SHEP9; agouti; agouti signal protein; agouti suppressor; | ||
| General Note | Ay is an old mutation propagated by mouse fanciers. In heterozygotes, all the hair pigment is yellow, but eyes are black. In combination with spotting genes, Ay usually causes reduction in size of white spots (J:12954, J:12035). Heterozygotes usually become obese and sterile after the first few months. Increased adipose tissue mass is due to fat cell hypertrophy. The amount of total body fat is higher than normal even when body weight is maintained at normal levels by restricted diet (J:5759). It has been hypothesized that the obesity in Ay/+ mice results from the observed reduction in hypothalamic norepinephrine and dopamine (J:3201). Heterozygotes are more susceptible to several kinds of tumors than normal mice, and their spleen cells cause a significantly lower graft vs. host reaction (J:5320). The level of malic enzyme in the liver is elevated (J:30972). Homozygotes die before implantation or shortly thereafter, the time of death and type of abnormality being in partdependent on the genetic background (J:5768). In embryos affected early, there is exclusion of some blastomeres from the embryo after the eight-cell stage (J:5650); in embryos affected later, abnormalities begin at implantation with failure of trophoblast giant cell development (J:14971). No single ultrastructural alteration characteristic of Ay/Ay pre-implantation embryos has been found (J:6010). The Ay mutation prolongs the period of embryonic sensitivity to hydrocortisone-induced cleft palate (J:4329). Ay/+ mutants have been used to test therapy for obesity and diabetes (J:1263). A report of recombination between Ay and the a and ax alleles suggested that Ay was a pseudoallele of the a locus on the proximal side (J:8877). However, cloning of the agouti locus and molecular analysis of a showed that the coding region of the two alleles is identical. The Ay mutation appears to be a DNA structural alteration that disrupts a gene (Raly) 5' to the agouti locus and places the agouti locus under the control of the Raly promotor. The pleiotropic effects of Ay are associated with the resulting deregulated overexpression of the agouti gene in numerous tissues of the adult animal. The recessive embryonic lethality in Ay mice may be due to lack of expression of Raly in the early embryo (J:12911). An ecotropic provirus (Emv15) is closely associated with the Ay mutation (J:6968), but has been separated from it in the YBR-Ay/a strain (J:8876, J:11956). | ||
| Molecular Note | The Ay mutation appears to be a DNA structural alteration that disrupts a gene, hnRNP associated with lethal yellow (Raly), 5' to the agouti locus and places the agouti locus under the control of the Raly promotor. [MGI Ref ID J:12911] [MGI Ref ID J:17512] [MGI Ref ID J:18921] | ||
Genotyping
Genotyping Information
This strain will not have a genotyping protocol or one is not currently available.
Helpful Links
Optimizing PCR Protocols
References
References
Selected Reference(s)
Diani AR; Sawada GA; Hannah BA; Jodelis KS; Connell MA; Connell CL; Vidmar TJ; Wyse BM. 1987. Analysis of pancreatic islet cells and hormone content in the spontaneously diabetic KKAy mouse by morphometry, immunocytochemistry and radioimmunoassay. Virchows Arch A Pathol Anat Histopathol 412(1):53-61. [PubMed: 2446417] [MGI Ref ID J:109946]
Robbins LS; Nadeau JH; Johnson KR; Kelly MA; Roselli-Rehfuss L; Baack E; Mountjoy KG; Cone RD. 1993. Pigmentation phenotypes of variant extension locus alleles result from point mutations that alter MSH receptor function. Cell 72(6):827-34. [PubMed: 8458079] [MGI Ref ID J:4636]
Additional References
Bouchard G; Johnson D; Carver T; Paigen B; Carey MC. 2002. Cholesterol gallstone formation in overweight mice establishes that obesity per se is not linked directly to cholelithiasis risk. J Lipid Res 43(7):1105-13. [PubMed: 12091495] [MGI Ref ID J:88773]
Bultman SJ; Klebig ML; Michaud EJ; Sweet HO; Davisson MT; Woychik RP. 1994. Molecular analysis of reverse mutations from nonagouti (a) to black-and-tan (a(t)) and white-bellied agouti (Aw) reveals alternative forms of agouti transcripts. Genes Dev 8(4):481-90. [PubMed: 8125260] [MGI Ref ID J:16984]
Bultman SJ; Michaud EJ; Woychik RP. 1992. Molecular characterization of the mouse agouti locus. Cell 71(7):1195-204. [PubMed: 1473152] [MGI Ref ID J:3523]
Chen Y; Duhl DM; Barsh GS. 1996. Opposite orientations of an inverted duplication and allelic variation at the mouse agouti locus. Genetics 144(1):265-77. [PubMed: 8878692] [MGI Ref ID J:35710]
Duhl DM; Stevens ME; Vrieling H; Saxon PJ; Miller MW; Epstein CJ; Barsh GS. 1994. Pleiotropic effects of the mouse lethal yellow (Ay) mutation explained by deletion of a maternally expressed gene and the simultaneous production of agouti fusion RNAs. Development 120(6):1695-708. [PubMed: 8050375] [MGI Ref ID J:18921]
Horvath TL; Diano S; Miyamoto S; Barry S; Gatti S; Alberati D; Livak F; Lombardi A; Moreno M; Goglia F; Mor G; Hamilton J; Kachinskas D; Horwitz B; Warden CH. 2003. Uncoupling proteins-2 and 3 influence obesity and inflammation in transgenic mice. Int J Obes Relat Metab Disord 27(4):433-42. [PubMed: 12664076] [MGI Ref ID J:82916]
Hustad CM; Perry WL; Siracusa LD; Rasberry C; Cobb L; Cattanach BM; Kovatch R; Copeland NG; Jenkins NA. 1995. Molecular genetic characterization of six recessive viable alleles of the mouse agouti locus. Genetics 140(1):255-65. [PubMed: 7635290] [MGI Ref ID J:24934]
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Klebig ML; Wilkinson JE; Geisler JG; Woychik RP. 1995. Ectopic expression of the agouti gene in transgenic mice causes obesity, features of type II diabetes, and yellow fur [see comments] Proc Natl Acad Sci U S A 92(11):4728-32. [PubMed: 7761391] [MGI Ref ID J:25738]
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Michaud EJ; Bultman SJ; Klebig ML; van Vugt MJ; Stubbs LJ; Russell LB; Woychik RP. 1994. A molecular model for the genetic and phenotypic characteristics of the mouse lethal yellow (Ay) mutation. Proc Natl Acad Sci U S A 91(7):2562-6. [PubMed: 8146154] [MGI Ref ID J:17512]
Michaud EJ; Bultman SJ; Stubbs LJ; Woychik RP. 1993. The embryonic lethality of homozygous lethal yellow mice (Ay/Ay) is associated with the disruption of a novel RNA-binding protein. Genes Dev 7(7A):1203-13. [PubMed: 8319910] [MGI Ref ID J:12911]
Michaud EJ; van Vugt MJ; Bultman SJ; Sweet HO; Davisson MT; Woychik RP. 1994. Differential expression of a new dominant agouti allele (Aiapy) is correlated with methylation state and is influenced by parental lineage. Genes Dev 8(12):1463-72. [PubMed: 7926745] [MGI Ref ID J:18848]
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]
Odaka H; Shino A; Ikeda H; Matsuo T. 1992. Antiobesity and antidiabetic actions of a new potent disaccharidase inhibitor in genetically obese-diabetic mice, KKA(y). J Nutr Sci Vitaminol (Tokyo) 38(1):27-37. [PubMed: 1629784] [MGI Ref ID J:1263]
Perry WL; Hustad CM; Swing DA; Jenkins NA; Copeland NG. 1995. A transgenic mouse assay for agouti protein activity. Genetics 140(1):267-74. [PubMed: 7635291] [MGI Ref ID J:24932]
Shimizu H; Uehara Y; Negishi M; Shimomura Y; Takahashi M; Fukatsu A; Takahashi S; Tanaka Y; Kashima K; Kobayashi I. 1992. Altered monoamine metabolism in the hypothalamus of the genetically obese yellow (Ay/a) mouse. Exp Clin Endocrinol 99(1):45-8. [PubMed: 1628697] [MGI Ref ID J:3201]
Siracusa LD; Russell LB; Eicher EM; Corrow DJ; Copeland NG; Jenkins NA. 1987. Genetic organization of the agouti region of the mouse. Genetics 117(1):93-100. [PubMed: 3666442] [MGI Ref ID J:8877]
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Vrieling H; Duhl DM; Millar SE; Miller KA; Barsh GS. 1994. Differences in dorsal and ventral pigmentation result from regional expression of the mouse agouti gene. Proc Natl Acad Sci U S A 91(12):5667-71. [PubMed: 8202545] [MGI Ref ID J:18750]
Xu B; Goulding EH; Zang K; Cepoi D; Cone RD; Jones KR; Tecott LH; Reichardt LF. 2003. Brain-derived neurotrophic factor regulates energy balance downstream of melanocortin-4 receptor. Nat Neurosci 6(7):736-42. [PubMed: 12796784] [MGI Ref ID J:84073]
Ay relatedAdachi Y; Yoshida J; Kodera Y; Kiss T; Jakusch T; Enyedy EA; Yoshikawa Y; Sakurai H. 2006. Oral administration of a zinc complex improves type 2 diabetes and metabolic syndromes. Biochem Biophys Res Commun 351(1):165-70. [PubMed: 17052688] [MGI Ref ID J:115628]
Adams SH; Won WB; Schonhoff SE; Leiter AB; Paterniti JR Jr. 2004. Effects of peptide YY[3-36] on short-term food intake in mice are not affected by prevailing plasma ghrelin levels. Endocrinology 145(11):4967-75. [PubMed: 15284202] [MGI Ref ID J:105614]
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Bouchard G; Johnson D; Carver T; Paigen B; Carey MC. 2002. Cholesterol gallstone formation in overweight mice establishes that obesity per se is not linked directly to cholelithiasis risk. J Lipid Res 43(7):1105-13. [PubMed: 12091495] [MGI Ref ID J:88773]
Bultman SJ; Michaud EJ; Woychik RP. 1992. Molecular characterization of the mouse agouti locus. Cell 71(7):1195-204. [PubMed: 1473152] [MGI Ref ID J:3523]
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Duhl DM; Stevens ME; Vrieling H; Saxon PJ; Miller MW; Epstein CJ; Barsh GS. 1994. Pleiotropic effects of the mouse lethal yellow (Ay) mutation explained by deletion of a maternally expressed gene and the simultaneous production of agouti fusion RNAs. Development 120(6):1695-708. [PubMed: 8050375] [MGI Ref ID J:18921]
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Fujimoto W; Shiuchi T; Miki T; Minokoshi Y; Takahashi Y; Takeuchi A; Kimura K; Saito M; Iwanaga T; Seino S. 2007. Dmbx1 is essential in agouti-related protein action. Proc Natl Acad Sci U S A 104(39):15514-9. [PubMed: 17873059] [MGI Ref ID J:125193]
Galbraith DB; Patrignani AM. 1976. Sulfhydryl compounds in melanocytes of yellow (Ay/a), nonagouti (a/a), and agouti (A/A) mice. Genetics 84(3):587-91. [PubMed: 1001879] [MGI Ref ID J:5737]
Gao J; Katagiri H; Ishigaki Y; Yamada T; Ogihara T; Imai J; Uno K; Hasegawa Y; Kanzaki M; Yamamoto TT; Ishibashi S; Oka Y. 2007. Involvement of apolipoprotein E in excess fat accumulation and insulin resistance. Diabetes 56(1):24-33. [PubMed: 17192461] [MGI Ref ID J:121950]
Garcia RJ; Ittah A; Mirabal S; Figueroa J; Lopez L; Glick AB; Kos L. 2008. Endothelin 3 induces skin pigmentation in a keratin-driven inducible mouse model. J Invest Dermatol 128(1):131-42. [PubMed: 17611578] [MGI Ref ID J:129906]
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Granholm DE; Reese RN; Granholm NH. 1996. Agouti alleles alter cysteine and glutathione concentrations in hair follicles and serum of mice (A y/a, A wJ/A wJ, and a/a). J Invest Dermatol 106(3):559-63. [PubMed: 8648194] [MGI Ref ID J:32132]
Granholm DE; Reese RN; Granholm NH. 1995. Agouti alleles influence thiol concentrations in hair follicles and extrafollicular tissues of mice (Ay/a, AwJ/AwJ, a/a). Pigment Cell Res 8(6):302-6. [PubMed: 8789738] [MGI Ref ID J:31403]
Grempler R; Zibrova D; Schoelch C; van Marle A; Rippmann JF; Redemann N. 2007. Normalization of prandial blood glucose and improvement of glucose tolerance by liver-specific inhibition of SH2 domain containing inositol phosphatase 2 (SHIP2) in diabetic KKAy mice: SHIP2 inhibition causes insulin-mimetic effects on glycogen metabolism, gluconeogenesis, and glycolysis. Diabetes 56(9):2235-41. [PubMed: 17596404] [MGI Ref ID J:126576]
Guo KY; Halo P; Leibel RL; Zhang Y. 2004. Effects of obesity on the relationship of leptin mRNA expression and adipocyte size in anatomically distinct fat depots in mice. Am J Physiol Regul Integr Comp Physiol 287(1):R112-9. [PubMed: 15001430] [MGI Ref ID J:109323]
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Health & husbandry
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Pricing, Supply Level & Notes, Controls, General Terms & Conditions
Pricing
| Pricing for USA, Canada and Mexico shipping destinations |
|
Weeks of Age Price* Gender Genotypes Provided Individual Mouse Price $101.80 Female or Male Heterozygous for Ay *Price(s) in US dollars ($)
Pairs /Price* Pair Genotype $154.05 Heterozygous for Ay x Wild-type for Ay
Additional Supply Details
| Supply Notes |
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| Pricing for International shipping destinations |
|
Weeks of Age Price* Gender Genotypes Provided Individual Mouse Price $132.40 Female or Male Heterozygous for Ay *Price(s) in US dollars ($)
Pairs /Price* Pair Genotype $200.30 Heterozygous for Ay x Wild-type for Ay
Additional Supply Details
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Supply Details
| Standard Supply | Repository-Live. A collection of over 1000 strains maintained as live colonies. Individual colonies are sized to meet current customer demand. Delivery for orders of 10 mice or less ranges on average from one to eight weeks; mice are generally shipped between four to six weeks of age with a maximum shipping age of ~nine weeks. Colony sizes do not generally support stringent age specifications for large volumes of mice; however custom orders and larger quantities of mice are easily arranged. Estimated ship dates for all orders provided within 48 hours of order placement. |
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| Supply Notes |
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Control Information
| Control | ||
|---|---|---|
| a/a 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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