Overview

Also Known As:KKAy, KK-Ay

Mice homozygous for the yellow spontaneous mutation (A^y) die before implantation or shortly thereafter. Heterozygotes usually become obese and infertile within a few months after birth. Heterozygotes are more susceptible to several kinds of tumors than are normal mice. Further, spleen cells from heterozygotes cause a significantly lower graft vs. host reaction. Mice of the KK strain develop diabetes of polygenic origin, and KK.Cg-A^y/J heterozygotes develop hyperglycemia, hyperinsulinemia, glucose intolerance and obesity by eight weeks of age. Pancreatic islets are hypertrophied and the β-cells are degranulated. Both the fat and lean tissue mass are increased compared to non-obese mice, with fat accounting for 30-35% of total body weight.

Genetic overview

Genetic Background	Generation
	Contact Technical Support (2018-07-27 00:00:00)

A^y

Allele Type	Gene Symbol	Gene Name
Spontaneous	a	nonagouti

View Genetics

Research Applications

Diabetes and Obesity Research
Dermatology Research
Endocrine Deficiency Research
Research Tools
Immunology, Inflammation and Autoimmunity Research
Internal/Organ Research
Reproductive Biology Research

View All Research Applications

Base Price

Starting at:

$142.48 Domestic price for male 3-week

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Details

Important Note

It has been reported that the KK strain is hemolytic complement deficient (Hc⁰), however, our strains have not been tested to confirm this allele. (Cinader B, et al.,2004, J Exp Med,120:897)

Detailed Description

A^y and other mutations at the a locus conferring a completely yellow coat color are dominant to all a alleles that produce a darker coat. Hair pigment of A^y heterozygotes is yellow, but eyes are black. Heterozygotes usually become obese and infertile within a few months after birth. Increased adipose tissue mass is due to fat cell hypertrophy, and it has been hypothesized that the obesity results from the observed reduction in hypothalamic norepinephrine and dopamine. Heterozygotes are more susceptible to several kinds of tumors than are normal mice, possibly due, at least in part, to a general increase in cell proliferation that also manifests as a slight increase in lean body mass and skeletal length. Further spleen cells from heterozygotes cause a significantly lower graft vs. host reaction. Mice homozygous for the yellow spontaneous mutation (A^y) 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. Mice of the KK strain develop diabetes of polygenic origin, and mice of other strains heterozygous for A^y become obese and mildly diabetic. KK.Cg-A^y/J heterozygotes develop hyperglycemia, hyperinsulinemia, glucose intolerance and obesity by eight weeks of age. Studies using isolated adipocytes indicate that tissue responsiveness to insulin is decreased. Histo- and immunocytochemical studies show that the pancreatic islets are hypertrophied and the β-cells are degranulated. These findings suggest that the principal cause of diabetes in these mice is insulin resistance. Body composition analysis shows that both the fat and lean tissue mass are increased compared to non-obese mice, with fat accounting for 30-35% of total body weight. The pleiotropic mutant phenotype of A^y/a mice is attributed to ectopic expression of the agouti protein, while the early embryonic lethality of the A^y mutation in the homozygous state is assumed to result from lack of expression of the Raly gene product (Bultman et al. 1992, Miller et al. 1993, Duhl et al. 1994, Michaud et al. 1993, 1994). That ectopic expression of the agouti protein is probably responsible for the non-lethal aspects of this mutation has been demonstrated by transgenic expression of the protein from a ubiquitous promoter (Klebig et al. 1995, Perry et al. 1995).

For further information, see Mouse Genome Informatics entries for a and for Raly and Michael F.W. Festing's description of KK.

Development

The A^y mutation was introduced onto the KK strain background by Dr. Nishimura in Japan. The Upjohn (Upj) colony of KK-A^y mice was initiated from mice acquired from Takeda Chemical Industries (Osaka, Japan) by Dr. George Gerritsen in 1983, at which time they had been inbred for 100 generations. The original KK-A^y strain was developed following initial crosses of A^y/a mice with mice of one of the inbred KK strains established from native Japanese mice (Kondo et al. 1957). As the diabetic characteristics of KK mice are generally considered to be of polygenic origin (Coleman 1982, Reddi and Camerini-Davalos 1988) and as Kondo established multiple sublines of KK mice, it is uncertain how closely related KK.Cg-A^y/J is to other KK strains. The Jackson Laboratory distributes the KK/HlJ (Stock No. 002106) obtained from Dr. Leiselotte Herberg at the Diabetes Research Institute in Dusseldorf, Germany. Additional backgrounds available: C57BL/6J-A^y.

Control Suggestions

Normal wildtype nonagouti (a/a) mice from the colony or KK/HlJ (Stock No. 002106) mice may be used as controls; the latter is only an approximate control whose degree of relationship to KK.Cg-A^y/J is uncertain (See Strain Development).
a/a from the colony

Additional Information

Considerations for Choosing Controls

Selected References

Reddi AS; Camerini-Davalos RA. 1988. Hereditary diabetes in the KK mouse: an overview. Adv Exp Med Biol 246:7-15PubMed: 3074669 MGI: J:109943
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):53-61PubMed: 2446417 MGI: J:109946
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):27-37PubMed: 1629784 MGI: J:1263
Iwatsuka H; Shino A; Suzuoki Z. 1970. General survey of diabetic features of yellow KK mice. Endocrinol Jpn 17(1):23-35PubMed: 5468422 MGI: J:26460

View All References

Genetics

A^y

Allele Symbol: A^y

Allele Name	agouti yellow
Allele Type	Spontaneous
Allele Synonym(s)	A^y; agouti yellow
Gene Symbol and Name	a, nonagouti
Gene Synonym(s)	agouti signal protein; As; ASP; As; agouti; agouti suppressor; AGTI; SHEP9; AGSW; AGTIL
Strain of Origin	old mutant of the mouse fancy
Chromosome	2
Molecular Note	The A^y 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. A report of recombination between A^y and the a and a^x alleles suggests that A^y was a pseudoallele of the a locus on the proximal side. However, cloning of the agouti locus and molecular analysis of a showed that the coding region of the three alleles is identical.

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Research Areas By Phenotype

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

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

Genotype: A^y related

Dermatology Research
- Color and White Spotting Defects
Endocrine Deficiency Research
- Adipose Defects
- Adrenal Cortex Defects
Research Tools
- Reproductive Biology Research
Diabetes and Obesity Research
- Obesity With Diabetes
Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency Associated with Other Defects
Internal/Organ Research
- Adipose Defects
- Adrenal Cortex Defects
Reproductive Biology Research
- Endocrine Deficiencies Affecting Gonads
- Fertility Defects

Mammalian Phenotype Terms by Genotype

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: A^y/A
involves: C57BL/6

adipose tissue phenotype

increased brown adipose tissue amount
- female mice have a 6-fold gain in weight of BAT compared to littermate controls

increased gonadal fat pad weight
- female mice have almost a 7-fold gain in weight of fat pad

increased inguinal fat pad weight
- female mice have a greater than 6-fold gain in weight of fat pad

increased percent body fat/body weight
- 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

increased retroperitoneal fat pad weight
- female mice have almost a 6-fold gain in weight of fat pad

homeostasis/metabolism phenotype

increased circulating leptin level
- circulating levels of leptin are over 12-fold higher compared to littermate controls

integument phenotype

yellow coat color
- mice have a yellow coat color

liver/biliary system phenotype

increased liver weight
- female mice have almost a 2-fold gain in weight of the liver

pigmentation phenotype

yellow coat color
- mice have a yellow coat color

behavior/neurological phenotype

hypoactivity
- the locomotor activity of mice is about half that of wild-type mice

increased food intake
- 18 week old mice eat about 1.4 times more food during a 7 day period compared to wild-type controls

growth/size/body region phenotype

increased body length
- female but not male mice have a significant 5% increase in their body length

increased susceptibility to weight gain
- mice gain weight at a greater rate than littermate controls starting at six weeks of age

obese
- by 23 weeks of age, female mice have almost double the weight compared to their wild-type littermate controls

Genotype: A^y/a
B6.Cg-A/J

behavior/neurological phenotype

abnormal food intake
- the stress of isolation, restraint, or ip injection inhibits feeding

integument phenotype

abnormal hair follicle melanogenesis
- decreased tyrosinase suggests the production of predominantly phaeomelanin (yellow)
- tyrosinase levels in hairbulb melanocytes ,as determined by 35S methionine incorporation and immunotitration, are reduced in comparison to a/a controls

pigmentation phenotype

abnormal hair follicle melanogenesis
- decreased tyrosinase suggests the production of predominantly phaeomelanin (yellow)
- tyrosinase levels in hairbulb melanocytes ,as determined by 35S methionine incorporation and immunotitration, are reduced in comparison to a/a controls

Genotype: A^y/A^y
101-A

cellular phenotype

maternal effect
- introducing homozygous A^y embryos into the uterus of a wild-type mouse delays embryonic death until after implantation begins
- there are approximately twice the number of cells, development of a small ectoplacental cone and Reichert's membrane, and disintegration of the decidual epithelium characteristic of an advanced implantation site

mortality/aging

embryonic lethality

embryonic lethality at implantation, complete penetrance
- putative homozygous embryos appear as small masses of vacuolated cells in decidual crypts at the time normal embryos are implanting; the abnormal embryo is resorbed within 36 hours
- Background Sensitivity - the genotype of the mother, with or without A^y, determines if a homozygous embryo dies at the initial stage of implantation or after the process begins

The following phenotype relates to a compound genotype created using this strain

Genotype: A^y/a
involves: KK

adipose tissue phenotype

increased total body fat amount
- adipose tissue weight increases with age, reaching a maximum at 10 weeks of age

renal/urinary system phenotype

abnormal renal glomerulus morphology
- some glomeruli exhibit an accumulation of eosinophilic material in the outer parts of the capillary

abnormal renal tubule morphology
- basement membrane of tubules is thickened
- hyaline materials or hyaline cast is present in tubules

dilated renal tubules

expanded mesangial matrix
- mesangial matrix is thickened

increased renal glomerulus basement membrane thickness
- basement membrane of Bowman's capsules is thickened

increased urine glucose level
- present at all ages tested (5, 10, 16 weeks) and in both sexes

renal cast
- hyaline materials or hyaline cast is present in tubules

endocrine/exocrine gland phenotype

abnormal pancreatic islet morphology
- central cavity formation with occasional red blood cells is observed in islets
- islets are hypertrophic in 10-16 week old mice

degranulated pancreatic beta cells
- beta cells are degranulated
- degranulated islets are infiltrated with fine glycogen granules

growth/size/body region phenotype

increased susceptibility to weight gain
- greater body weight gain occurs in females as compared to black KK controls

homeostasis/metabolism phenotype

abnormal lipid homeostasis
- 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
- blood glucose levels increase with age in both sexes
- marked hyperglycemia (400-500 mg/dl) develops by 16 weeks of age

impaired glucose tolerance

increased circulating insulin level
- markedly elevated plasma immunoreactive insulin (IRI) level increases with age

increased urine glucose level
- present at all ages tested (5, 10, 16 weeks) and in both sexes

insulin resistance
- insulin sensitivity is impaired at 10 weeks and lost by 16 weeks

Phenotype Information

Body Weight, Glucose, Glucose Tolerance, and Other Phenotypes

References

Reddi AS; Camerini-Davalos RA. 1988. Hereditary diabetes in the KK mouse: an overview. Adv Exp Med Biol 246:7-15PubMed: 3074669 MGI: J:109943
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):53-61PubMed: 2446417 MGI: J:109946
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):27-37PubMed: 1629784 MGI: J:1263
Iwatsuka H; Shino A; Suzuoki Z. 1970. General survey of diabetic features of yellow KK mice. Endocrinol Jpn 17(1):23-35PubMed: 5468422 MGI: J:26460

Additional References

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):1203-13PubMed: 8319910 MGI: J:12911
Bleasdale JE; Swanson ML. 1993. Hepatic insulin resistance in KKA(y) mice and its amelioration by pioglitazone do not involve alterations in phospholipase C activity. Biochim Biophys Acta 1181(3):240-8PubMed: 8391325 MGI: J:14378
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):481-90PubMed: 8125260 MGI: J:16984
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):2562-6PubMed: 8146154 MGI: J:17512
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):5667-71PubMed: 8202545 MGI: J:18750
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):1463-72PubMed: 7926745 MGI: J:18848
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):1695-708PubMed: 8050375 MGI: J:18921
Meglasson MD; Wilson JM; Yu JH; Robinson DD; Wyse BM; de Souza CJ. 1993. Antihyperglycemic action of guanidinoalkanoic acids: 3-guanidinopropionic acid ameliorates hyperglycemia in diabetic KKAy and C57BL6Job/ob mice and increases glucose disappearance in rhesus monkeys. J Pharmacol Exp Ther 266(3):1454-62PubMed: 8371149 MGI: J:21357
Perry WL; Hustad CM; Swing DA; Jenkins NA; Copeland NG. 1995. A transgenic mouse assay for agouti protein activity. Genetics 140(1):267-74PubMed: 7635291 MGI: J:24932
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):255-65PubMed: 7635290 MGI: J:24934
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):4728-32PubMed: 7761391 MGI: J:25738
Cheng Y; Yu X; Zhang J; Chang Y; Xue M; Li X; Lu Y; Li T; Meng Z; Su L; Sun B; Chen L. 2019. Pancreatic kallikrein protects against diabetic retinopathy in KK Cg-A(y)/J and high-fat diet/streptozotocin-induced mouse models of type 2 diabetes. Diabetologia 62(6):1074-1086PubMed: 30838453 MGI: J:280268
Huby AC; Otvos L Jr; Belin de Chantemele EJ. 2016. Leptin Induces Hypertension and Endothelial Dysfunction via Aldosterone-Dependent Mechanisms in Obese Female Mice. Hypertension 67(5):1020-8PubMed: 26953321 MGI: J:280721
Morgan DA; Rahmouni K. 2010. Differential effects of insulin on sympathetic nerve activity in agouti obese mice. J Hypertens 28(9):1913-9PubMed: 20577122 MGI: J:281412
Gonzalez C; Silva-Ramirez AS; Navarro-Tovar G; Barrios-Capuchino JJ; Rocha-Uribe A. 2020. Effect of the double bond conjugation on the vascular physiology and nitric oxide production of isomers of eicosapentaenoic and docosahexaenoic acids prepared from shark oil. PLoS One 15(2):e0229435PubMed: 32107491 MGI: J:285951
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):45-8PubMed: 1628697 MGI: J:3201
Bultman SJ; Michaud EJ; Woychik RP. 1992. Molecular characterization of the mouse agouti locus. Cell 71(7):1195-204PubMed: 1473152 MGI: 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):265-77PubMed: 8878692 MGI: J:35710
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):454-67PubMed: 8449404 MGI: J:4186
Shafrir E. 1992. Animal models of non-insulin-dependent diabetes. Diabetes Metab Rev 8(3):179-208PubMed: 1292911 MGI: J:4453
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):827-34PubMed: 8458079 MGI: J:4636
Herberg L; Coleman DL. 1977. Laboratory animals exhibiting obesity and diabetes syndromes. Metabolism 26(1):59-99PubMed: 834144 MGI: J:5759
Wu C; Okar DA; Newgard CB; Lange AJ. 2002. Increasing fructose 2,6-bisphosphate overcomes hepatic insulin resistance of type 2 diabetes. Am J Physiol Endocrinol Metab 282(1):E38-45PubMed: 11739081 MGI: J:75519
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):93-100PubMed: 3666442 MGI: J:8877
Ye G; Metreveli NS; Donthi RV; Xia S; Xu M; Carlson EC; Epstein PN. 2004. Catalase protects cardiomyocyte function in models of type 1 and type 2 diabetes. Diabetes 53(5):1336-43PubMed: 15111504 MGI: J:89389

Additional - A^y related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Separated PCR:A A A
- Separated PCR:A A A Alternate2
- Genotyping resources and troubleshooting
Coat color is used to determine genotypes of our KK.Cg-A^y/J colony. Black (a/a homozygous) females are bred to yellow (A^y/a) males. All offspring with the A^y/a mutation and phenotype are yellow, the wild-type mice are black.
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

This strain is a challenging breeder.

All yellow (A^y/a) male breeders are confirmed to be diabetic at 13 weeks of age (non-fasting blood glucose exceeding 300 mg/dL) and weigh either 32 grams at 13 weeks of age or 33 grams at 14 weeks of age.
- Additional Breeding and Husbandry Support
Mating System
- +/+ sibling x Heterozygote
Appearance
- yellow, affected
  Related Genotype: A^y/a
  
  black, unaffected
  Related Genotype: a/a
Citation
When using the KK.Cg-A^y/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #002468 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

AX27 (Maximum)

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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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Also Known As:KKAy, KK-Ay

Genetic overview

Research Applications

Base Price

Important Note

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Ay

Allele Symbol: Ay

Disease Terms

Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).

Research Areas By Phenotype

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

Genotype: Ay related

Mammalian Phenotype Terms by Genotype

Genotype: Ay/Ainvolves: C57BL/6

adipose tissue phenotype

homeostasis/metabolism phenotype

integument phenotype

liver/biliary system phenotype

pigmentation phenotype

behavior/neurological phenotype

growth/size/body region phenotype

Genotype: Ay/aB6.Cg-A/J

behavior/neurological phenotype

integument phenotype

pigmentation phenotype

Genotype: Ay/Ay101-A

cellular phenotype

mortality/aging

Genotype: Ay/ainvolves: KK

adipose tissue phenotype

renal/urinary system phenotype

endocrine/exocrine gland phenotype

growth/size/body region phenotype

homeostasis/metabolism phenotype

Phenotype Information

References

Additional References

Additional - Ay related

Genotyping Protocols

Dietary Information

Breeding Considerations

Mating System

Appearance

Citation

Animal Health Reports

Live Mouse

Cryorecovery - Pricing

Payment Terms and Conditions

The Jackson Laboratory's Genotype Promise

Terms Of Use

Licensing Information

JAX® Mice, Products & Services Conditions of Use

No Warranty

Credit for PRODUCTS or SERVICES

Animal Care and Use for SERVICES

No Liability

A^y

Allele Symbol: A^y

Genotype: A^y related

Genotype: A^y/A
involves: C57BL/6

Genotype: A^y/a
B6.Cg-A/J

Genotype: A^y/A^y
101-A

Genotype: A^y/a
involves: KK

Additional - A^y related