A<y> Spontaneous Allele Detail MGI Mouse (MGI:1856798)

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A^y
Spontaneous Allele Detail

Nomenclature | Mutation origin | Mutation description | Find Mice (IMSR) | Expression | Phenotype summary | Phenotypes by genotype | Disease models | Notes | References

Nomenclature

Symbol:	A^y
Name:	nonagouti; agouti yellow
MGI ID:	MGI:1856798
Synonyms:	A(y), Ay
Gene:	a Location: Chr2:154617138-154876748 bp, + strand Genetic Position: Chr2, 89.0 cM

A^y/a mouse

Show the 4 image(s) involving this allele.

Mutation
origin

Strain of Origin:

old mutant of the mouse fancy

Mutation
description

Allele Type:	Spontaneous
Mutation:	Other
	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. (J:12911, J:17512, J:18921)
Inheritance:	Semidominant

Find Mice (IMSR)

Mouse strains and cell lines available from the International Mouse Strain Resource (IMSR)

Carrying this Mutation:	Mouse Strains: 10 strains available Cell Lines: 0 lines available
Carrying any a Mutation:	314 strains or lines available

Expression

In Mice Carrying this Mutation:

8 assay results

Phenotype
summary

Phenotype Summary by Mammalian Phenotype terms

(show or hide all annotated terms)

Genotypes are listed in the next section.

Key:

hm	homozygous	ht	heterozygous
cn	conditional genotype	cx	complex: > 1 genome feature
tg	involves transgenes	ot	other: hemizygous, indeterminate,...
N	normal phenotype		expected model not found

Affected Systems

Genotypes:

adipose tissue

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behavior/neurological

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craniofacial

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digestive/alimentary system

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endocrine/exocrine glands

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growth/size

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homeostasis/metabolism

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liver/biliary system

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pigmentation

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renal/urinary system

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skeleton

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skin/coat/nails

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tumorigenesis

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Disease Models

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Phenotypic
data by
genotype

Phenotypic Data by Genotype

(show or hide all phenotypic details)

Genotype

Allelic Composition

Genetic Background

129S1.C3-A^y/A^w Chr 19^MOLF/Ei

B6.Cg-A^y/J

ht3 Disease Model

involves: C57BL/6

ht4 Disease Model

involves: KK

A^y/a
Npbwr1^tm1Rck/Npbwr1^tm1Rck

involves: 129P/Ola * C57BL/6J

A^y/a
Agrp^tm2(DTR)Rpa/Agrp⁺

involves: 129S4/SvJaeSor * KK/Upj

A^y/A
Prkar2b^tm2Gsm/Prkar2b^tm2Gsm

involves: C57BL/6

A^y/A
Prkar2b^tm2Gsm/Prkar2b⁺

involves: C57BL/6

a/A^y
Zc3h4^KK/Zc3h4^KK

involves: C57BL/6J * KK-A^y

a/A^y
Zc3h4^C57BL/6J/Zc3h4^KK

involves: C57BL/6J * KK-A^y

a/A^y
Bwq2^KK/Bwq2^KK

involves: C57BL/6J * KK-A^y

a/A^y
Bwq10^C57BL/6J/Bwq10^C57BL/6J

involves: C57BL/6J * KK-A^y

a/A^y
Guq1^KK/Guq1^KK

involves: C57BL/6J * KK-A^y

a/A^y
Guq2^C57BL/6J/Guq2^C57BL/6J

involves: C57BL/6J * KK-A^y

A^y/a
Mssq1^KK/TaJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq2^C57BL/6JJcl/Mssq2^KK/TaJcl

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq3^KK/TaJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq4^KK/TaJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq5^C57BL/6JJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq6^C57BL/6JJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq6^KK/TaJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq7^KK/TaJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq9^C57BL/6JJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq10^KK/TaJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq11^KK/TaJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq12^KK/TaJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq13^KK/TaJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq13^C57BL/6JJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq14^KK/TaJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Mssq16^KK/TaJcl/?

involves: C57BL/6JJcl * KK/TaJcl

A^y/a
Dmbx1^tm1Sse/Dmbx1^tm1Sse

involves: ICR

A^y/a
Tyrp1^B-lt/?

Not Specified

Disease
models

Mouse Models of Human Disease		Note	Genotype			Ref(s)
				Allelic Composition	Genetic Background
Models with phenotypic similarity to human diseases not associated with human ASIP.
Diabetes Mellitus, Noninsulin-Dependent; NIDDM OMIM ID: 125853			ht4	A^y/a	involves: KK	J:26460
Obesity OMIM ID: 601665			ht3	A^y/A	involves: C57BL/6	J:131039

Notes

A^y 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, A^y 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 A^y/+ 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 part dependent 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 A^y/A^y pre-implantation embryos has been found (J:6010). The A^y mutation prolongs the period of embryonic sensitivity to hydrocortisone-induced cleft palate (J:4329). A^y/+ mutants have been used to test therapy for obesity and diabetes (J:1263). A report of recombination between A^y and the a and a^x alleles suggested that A^y 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 A^y 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 A^y are associated with the resulting deregulated overexpression of the agouti gene in numerous tissues of the adult animal. The recessive embryonic lethality in A^y 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 A^y mutation (J:6968), but has been separated from it in the YBR-A^y/a strain (J:8876, J:11956).

References

Original:	J:12954 Dunn LC et al., "Studies on Spotting Patterns III. Interaction between Genes Affecting White Spotting and Those Affecting Color in the House Mouse." Genetics 1937 Mar;22(2):307-18
All:	130 reference(s)

Contributing Projects: Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
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