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Strain Name:

B6.Cg-Ay/J

Stock Number:

000021

Availability:

Repository- Live

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General Terms and Conditions

Genes & Alleles   Ay;   a;

Product Information

Strain Details

Type JAX® GEMM® Strain - Congenic
Additional information on JAX® GEMM® Strains.
Type JAX® GEMM® Strain - Mutant Strain
Specieslaboratory mouse
Background Strain C57BL/6J
Donor Strain Fancier
H2 Haplotypeb
GenerationF88 (21-JAN-08)

Appearance
yellow, affected
Related Genotype: Ay/a

black, unaffected
Related Genotype: a/a

Strain Description
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.

Related Disease (OMIM) Terms

Diabetes Mellitus, Noninsulin-Dependent; NIDDM
Mammalian Phenotype Terms 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

Gene & Allele Details

Allele Symbol Ay
Allele Name yellow
Common Name(s) A(y); Ay;
Strain of Originold 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]

Control Information

  Control
   a/a from the colony
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Colony Maintenance

Diet Information LabDiet® 5K54

Related Strains

Strains carrying   Ay allele
005505   B6.Cg-Ay Slc7a11sut/LmLlp
002468   KK.Cg-Ay/J
View Strains carrying   Ay     (2 strains)

Strains carrying other alleles of a
003301   (C57BL/6J x C3H-Eya1bor)F1/J
000251   AEJ.Cg-ae +/a Gdf5bp-H/J
000202   AEJ/Gn-bd/J
000199   AEJ/GnLeJ
000427   B10.CE-H13b Aw/(30NX)SnJ
000420   B10.LP-H13b Aw/Sn
000477   B10.PA-Pldnpa H3e at/SnJ
000419   B10.UW-H3b we Pax1un at/SnJ
003879   B10;TFLe-a/a T tf/+ tf/J
001538   B6 x B6C3Sn a/A-T(1;9)27H/J
000916   B6 x B6C3Sn a/A-T(5;12)31H/J
000602   B6 x B6C3Sn a/A-T(8;16)17H/J
000593   B6 x B6CBCa Aw-J/A-Grid2Lc T(2;6)7Ca MitfMi-wh/J
000502   B6 x B6CBCa Aw-J/A-Myo5aflr Gnb5flr/J
000599   B6 x B6CBCa Aw-J/A-T(5;13)264Ca KitW-v/J
002083   B6 x B6EiC3 a/A-T(7;16)235Dn/J
000507   B6 x B6EiC3 a/A-Otcspf/J
000618   B6 x FSB/GnEi a/a Ctslfs/J
000577   B6 x STOCK a Oca2p Hps5ru2 Ednrbs/J
000601   B6 x STOCK a/a T(7;18)50H/J
000592   B6 x STOCK T(2;4)13H a/J
002016   B6(Cg)-Aw-J EdaTa-6J Chr YB6-Sxr/EiJ
000552   B6-Aw-J-EdaTa-6J.Cg-Sxr
001730   B6-Aw-J-EdaTa-6J.Cg-Sxrb Hya-/J
000841   B6-Aw-J.CBy-EdaTa-By/J
001809   B6-Aw-J.Cg-EdaTa-6J +/+ ArTfm/J
000600   B6-Gpi1b x B6CBCa Aw-J/A-T(7;15)9H Gpi1a/J
000769   B6.C/(HZ18)By-at-44J/J
000001   B6.C3 A/a Mgrn1md/J
000203   B6.C3-Aiy/a/J
000017   B6.C3Fe-Avy/J
000628   B6.CE-A Amy1b Amy2b/J
001572   B6.Cg-am-J/J
100409   B6129PF1/J-Aw-J/Aw
004200   B6;CBACa Aw-J/A-Npr2cn-2J/J
000785   B6;D2-a Es1e/J
000505   B6C3 Aw-J/A-Mutedmu/J
000604   B6C3 a/A-T(10;13)199H +/+ Lystbg-J/J or Lystbg-2J/J
002807   B6C3Fe a/a-Meox2fla/J
000224   B6C3Fe a/a-Scyl1mdf/J
001037   B6C3Fe a/a-Agtpbp1pcd/J
000221   B6C3Fe a/a-Alx4lst-J/J
002062   B6C3Fe a/a-Atp7aMo-8J/J
001756   B6C3Fe a/a-Cacng2stg/J
001815   B6C3Fe a/a-Col1a2oim/J
000231   B6C3Fe a/a-Csf1op/J
000209   B6C3Fe a/a-Dh/J
000211   B6C3Fe a/a-Dstdt-J/J
000210   B6C3Fe a/a-Edardl-J/J
000207   B6C3Fe a/a-Edaraddcr/J
000182   B6C3Fe a/a-Eef1a2wst/J
001278   B6C3Fe a/a-Glra1spd/J
000241   B6C3Fe a/a-Glrbspa/J
002875   B6C3Fe a/a-Hoxd13spdh/J
000304   B6C3Fe a/a-Krt71Ca Scn8amed-J/J
000226   B6C3Fe a/a-Largemyd/J
000636   B6C3Fe a/a-Lmx1adr-J/J
001280   B6C3Fe a/a-Lse/J
001573   B6C3Fe a/a-MitfMi/J
001035   B6C3Fe a/a-Napahyh/J
000181   B6C3Fe a/a-Otogtwt/J
000278   B6C3Fe a/a-Papss2bm Hps1ep Hps6ru/J
000205   B6C3Fe a/a-Papss2bm/J
002078   B6C3Fe a/a-Pcdh15av-2J/J
000246   B6C3Fe a/a-Pitpnavb/J
001430   B6C3Fe a/a-Ptch1mes/J
000506   B6C3Fe a/a-Qkqk/J
000235   B6C3Fe a/a-Relnrl/J
000237   B6C3Fe a/a-Rorasg/J
000290   B6C3Fe a/a-Sox10Dom/J
000230   B6C3Fe a/a-Tcirg1oc/J
003612   B6C3Fe a/a-Trak1hyrt/J
001512   B6C3Fe a/a-Ttnmdm/J
001607   B6C3Fe a/a-Unc5crcm/J
000005   B6C3Fe a/a-Wc/J
000243   B6C3Fe a/a-Wnt1sw/J
000248   B6C3Fe a/a-Xpl/J
001750   B6C3Fe a/a-XsJ/J
000624   B6C3Fe a/a-anx/J
003020   B6C3Fe a/a-dep/J
002018   B6C3Fe a/a-din/J
002339   B6C3Fe a/a-nma/J
000240   B6C3Fe a/a-soc/J
000063   B6C3Fe a/a-sy/J
001055   B6C3Fe a/a-tip/J
000245   B6C3Fe a/a-tn/J
000065   B6C3Fe a/a-we Pax1un at/J
000296   B6C3Fe-a/a Hoxa13Hd Mcoln3Va-J/J
000019   B6C3Fe-a/a-Itpr1opt/J
001022   B6C3FeF1/J a/a
000314   B6CBACa Aw-J/A-EdaTa/J-XO
000501   B6CBACa Aw-J/A-Aifm1Hq/J
001046   B6CBACa Aw-J/A-Grid2Lc/J
000500   B6CBACa Aw-J/A-Gs/J
002703   B6CBACa Aw-J/A-Hydinhy3/J
000247   B6CBACa Aw-J/A-Kcnj6wv/J
000287   B6CBACa Aw-J/A-Plp1jp EdaTa/J
000515   B6CBACa Aw-J/A-SfnEr/J
000242   B6CBACa Aw-J/A-spc/J
000288   B6CBACa Aw-J/A-we a Mafbkr/J
001201   B6CBACaF1/J-Aw-J/A
001752   B6CBCa Aw-J/A-T(7;15)9H/J
000971   B6EiC3 a/A-Och/J
000551   B6EiC3 a/A-Tbx15de-H/J
006450   B6EiC3 a/A-Vss/J
000557   B6EiC3-+ a/LnpUl A/J
000504   B6EiC3Sn a/A-Cacnb4lh/J
000553   B6EiC3Sn a/A-Egfrwa2 Wnt3avt/J
000503   B6EiC3Sn a/A-Gy/J
001811   B6EiC3Sn a/A-Otcspf-ash/J
002343   B6EiC3Sn a/A-Otcspf/J
000391   B6EiC3Sn a/A-Pax6Sey-Dey/J
001924   B6EiC3Sn a/A-Ts(1716)65Dn
001923   B6EiC3Sn a/A-Ts(417)2Lws Tim/J
000200   C3FeB6 A/Aw-J-Ankank/J
000638   C3FeB6 A/Aw-J-Spnb4qv-J/J
001203   C3FeB6F1/J A/Aw-J
000225   C3FeLe.B6 a/a-Ptpn6me/J
000198   C3FeLe.B6-a/J
000291   C3FeLe.Cg-a/a Hm KitlSl Krt71Ca-J/J
001272   C3H/HeSnJ-Ahvy/J
000099   C3HeB/FeJ-Avy/J
001886   C3HeB/FeJLe a/a-gnd/J
000338   C57BL/6J Aw-J-EdaTa-6J/J
000584   C57BL/6J-+ T(1;2)5Ca/a +/J
000258   C57BL/6J-Ai/a/J
000774   C57BL/6J-Asy/a/J
000569   C57BL/6J-Aw-J-EdaTa +/+ ArTfm/J
000051   C57BL/6J-Aw-J/J
000055   C57BL/6J-at-33J/J
000070   C57BL/6J-atd/J
000284   CWD/LeJ
000670   DBA/1J
000671   DBA/2J
001057   HPT/LeJ
000260   JGBF/LeJ
000262   LS/LeJ
000283   LT.CAST-A/J
000265   MY/HuLeJ
000308   SSL/LeJ
001759   STOCK A Tyrc Sha/J
001427   STOCK Aw us/J
000994   STOCK a Myo5ad Mregdsu/J
000064   STOCK a Tyrp1b Sisi/J
002238   STOCK a Tyrp1b shmy/J
001433   STOCK a skt/J
000579   STOCK a tp/J
000319   STOCK a us/J
002648   STOCK a/a Cln6nclf/J
000317   STOCK a/a Egfrwa2/J
000302   STOCK a/a MitfMi-wh +/+ Itpr1opt/J
000286   STOCK a/a Myo5ad fd/+ +/J
000206   STOCK a/a Tyrc-h/J
001432   STOCK a/a Tyrp1b sks/Tyrp1b +/J
000281   STOCK a/a ma ft/ma ft/J
000312   STOCK stb + a/+ Fignfi a/J
000596   STOCK T(2;11)30H/+ x AEJ-a Gdf5bp-H/J or A/J-a Gdf5bp-J/J
000970   STOCK T(2;16)28H A/T(2;16)28H a/J
000590   STOCK T(2;4)1Sn a/J
000594   STOCK T(2;8)26H a/T(2;8)26H a Tyrp1+/Tyrp1b/J
000623   TR/DiEiJ
View Strains carrying other alleles of a     (161 strains)

Additional Web Information

Congenic Nomenclature
Genetic Quality Control Annual Report

Animal Health Reports

Room Number           FGB27

Research Applications

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

Diabetes and Obesity Research
Hyperglycemia
Hyperinsulinemia
Insulin Resistance
Type 2 Diabetes (NIDDM)

Ay related

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

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

Price and Supply Information

Strain Name: B6.Cg-Ay/J
Stock Number: 000021

Price Details

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Supply Details

Standard SupplyRepository-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.
Supply Notes Usually shipped between four and eight weeks of age.
This strain is included in the Special Mutant Stock Resource collection.
Genomic DNA is available for this strain from the Mouse DNA Resource.
LicensingSee General Terms and Conditions below  
Control InformationView Control Information in Strain Details.

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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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