Overview

Mice homozygous for the hr spontaneous mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of stratified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. HRS/J mice, fed an ather...

Genetic overview

Genetic Background	Generation

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Research Applications

Cancer Research
Dermatology Research
Immunology, Inflammation and Autoimmunity Research
Cardiovascular Research
Mouse/Human Gene Homologs
Research Tools

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Base Price

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$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Mice homozygous for the hr spontaneous mutation have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. Deficiency of splenic T helper cells (Ly-1+) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hr/hr mice up to 10 days but then hair is lost from the follicle. Waves of hair growth with few thin fuzzy hairs ocur at monthly intervals for some time but homozygotes eventually become continuously hairless. Vibrissae are repeatedly regrown and shed, becoming more abnormal with age. Toenails are long and curved. There is hyperkeratosis of stratified epithelium and the upper part of hair canals beginning at 14 days. Hair club formation is abnormal. Cysts form from the hyperkeratotic upper part of hair canals and sheaths of abnormal follicles stranded in dermis. Some cysts also form from sebaceous glands. All cysts undergo sebaceous transformation and later keratinization. HRS/J mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice (e.g. C57BL/6J, Stock No. 000664; C57L/J, Stock No. 000668, C57BR/cdJ, Stock No. 000667, and SM/J, Stock No. 000687).

Development

The hairless mutation (Hr^hr) was found in a mouse caught in an aviary in London in 1924. It was brought to The Jackson Laboratory in 1956 by Dr. E. L. Green who had received it from Dr. H. Chase at Brown University in 1952. Dr. Green crossed it to a BALB/c female and the stock was sibling mated. The genotype was fixed homozygous for brown (Tyrp1^b), albino (Tyr^c), dilute (Myo5a^d) and kept segregating for hairless. Since the hairless females do not nurse their litters it was bred hairless males x haired females. In 1964 at generation F24 the strain was named HRS/J. Embryos were cryopreserved in 1992 from haired females mated to hairless males at F90.

Control Suggestions

Heterozygote from the colony

Additional Information

Considerations for Choosing Controls

Genetics

Ahr^b-2

Allele Symbol: Ahr^b-2

Allele Name	b-2 variant
Allele Type	Not Applicable
Allele Synonym(s)	Ah^b-2; Ah^h
Gene Symbol and Name	Ahr, aryl-hydrocarbon receptor
Gene Synonym(s)
Strain of Origin	BALB/cBy
Chromosome	12
General Note	C57BL/6 carries the responsive Ahr^b allele; DBA/2 carries nonresponsive Ahr^d. Heterozygotes (Ahr^b/Ahr^d) are responsive (J:5282). Later work identified a second (J:8895) and later a third (J:22144) allele conferring response. Thus the allele in C57, C58, and MA/My strains is now Ahr^b-1; Ahr^b-2 is carried by BALB/cBy, A, and C3H; and Ahr^b-3 by Mus spretus, M. caroli, and MOLF/Ei. The nonresponsive strains AKR, DBA/2, and 129 carry Ahrd (J:22144). Nucleotide and amino acid sequence differences between Ahr^b-1 and Ahr^d have been determined (J:17460). Strain of origin - this allele was found in BALB/cByJ, A/J, C3H/HeJ, CBA strains
Molecular Note	This allele encodes a high affinity, heat labile, 104 kDa receptor containing 848 amino acids. Sequencing studies of cDNA from C57BL/6J congenic mice homozygous for this allele identified nucleotide substitutions in the ORF that would cause 5 amino acid differences between the C57BL/6J and BALB/cBy peptides, and 2 amino acid differences between the BALB/cBy and DBA/2J peptides. A T to C transition in exon 11 replaces the opal termination codon in the C57BL/6J allele with an arginine codon in the BALB/cBy allele. This change would extend translation of the BALB/cBy mRNA by 43 amino acids, accounting for the larger size of the peptide produced by this allele (104 kDa, vs 95 kDa for the C57BL/6J allele).

Hr^hr

Allele Symbol: Hr^hr

Allele Name	hairless
Allele Type	Spontaneous
Allele Synonym(s)	hr; SKH-1
Gene Symbol and Name	Hr, lysine demethylase and nuclear receptor corepressor
Gene Synonym(s)
Strain of Origin	Not Specified
Chromosome	14
Molecular Note	The hr allele is the result of a retroviral integration. Insertion of murine leukemia proviral sequences into intron 6 results in aberrant splicing of the gene.

Myo5a^d

Allele Symbol: Myo5a^d

Allele Name	dilute
Allele Type	Spontaneous
Allele Synonym(s)	blue dilution; d; d^v; Maltese dilution
Gene Symbol and Name	Myo5a, myosin VA
Gene Synonym(s)
Strain of Origin	old mutant of the mouse fancy
Chromosome	9
Molecular Note	This mutation is the result of the integration of ecotropic murine leukemia virus Emv-3 into a noncoding region of the Myo5a^d gene. Reversions of Myo5a^d to wild-type are caused by excision of the virus leaving exactly one long terminal repeat in place.

Disease/Phenotype

Disease Terms

Research Areas By Phenotype

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

Genotype: Hr^hr related

Cancer Research
- Toxicology
- Increased Tumor Incidence
  - Leukemia: lymphocytic
  - Lymphomas: thymic
  - Skin Cancers: Induced
  - Leukemia
  - Lymphomas
  - Skin Cancers
Dermatology Research
- Skin and Hair Texture Defects
Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency Associated with Other Defects
Cardiovascular Research
- Diet-Induced Atherosclerosis
  - Relatively Resistant
Research Tools
- Toxicology Research
  - drug/compound testing

Genotype: Myo5a^d related

Mouse/Human Gene Homologs
- Griscelli Syndrome
Dermatology Research
- Color and White Spotting 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: Hr^hr/Hr^hr
Not Specified

behavior/neurological phenotype

abnormal nursing
- failure

endocrine/exocrine gland phenotype

abnormal mammary gland morphology
- nipple at bottom of cup-shaped depression in skin
- no ducts
- small

sebaceous gland atrophy

integument phenotype

abnormal dermis reticular layer morphology
- cystic

abnormal mammary gland morphology
- nipple at bottom of cup-shaped depression in skin
- no ducts
- small

abnormal skin morphology
- thickened cutis

deformed nails
- curved

dermal cysts

epidermal hyperplasia

hairless
- beginning ~15 days of age and progressing from nose back

hyperkeratosis

sebaceous gland atrophy

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

Genotype: Hr^hr/Hr^hr
HRS/J

cellular phenotype

decreased T cell proliferation
- to alloantigens by T helper cells

hearing/vestibular/ear phenotype

absent linear vestibular evoked potential
- VESPs are absent at the maximum stimulus intensity used

hematopoietic system phenotype

decreased T cell number
- of CD5+ T cells

decreased T cell proliferation
- to alloantigens by T helper cells

increased macrophage cell number
- although heterozygotes and homozygotes have the same total number of peritoneal cells, the percentage expressing Mac-1 is an average of 30% in homozygotes versus an average of 14% in heterozygotes

immune system phenotype

decreased T cell number
- of CD5+ T cells

decreased T cell proliferation
- to alloantigens by T helper cells

increased macrophage cell number
- although heterozygotes and homozygotes have the same total number of peritoneal cells, the percentage expressing Mac-1 is an average of 30% in homozygotes versus an average of 14% in heterozygotes

neoplasm

increased leukemia incidence
- at 8 to 10 months of age 45% of homozygotes have lymphoid leukemia, compared with only 1% in heterozygotes, and approximately 72% of these homozygotes develop myeloid leukemia later in life up to 18 months of age
- increased incidence

References

Additional References

Cachon-Gonzalez MB; Fenner S; Coffin JM; Moran C; Best S; Stoye JP. 1994. Structure and expression of the hairless gene of mice. Proc Natl Acad Sci U S A 91(16):7717-21PubMed: 8052649 MGI: J:19624
Morrissey PJ; Parkinson DR; Schwartz RS; Waksal SD. 1980. Immunologic abnormalities in HRS/J mice. I. Specific deficit in T lymphocyte helper function in a mutant mouse. J Immunol 125(4):1558-62PubMed: 6447727 MGI: J:6375
Poland A; Glover E. 1990. Characterization and strain distribution pattern of the murine Ah receptor specified by the Ahd and Ahb-3 alleles. Mol Pharmacol 38(3):306-12PubMed: 2169579 MGI: J:34840
Reske-Kunz AB; Scheid MP; Boyse EA. 1979. Disproportion in T-cell subpopulations in immunodeficient mutant hr/hr mice. J Exp Med 149(1):228-33PubMed: 310859 MGI: J:6087

Additional - Ahr^b-2 related

Additional - Hr^hr related

Additional - Myo5a^d related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Separated PCR:Hr
- Genotyping resources and troubleshooting
Appearance
- unpigmented, without hair
  Related Genotype: Tyrp1^b/Tyrp1^b Tyr^c/Tyr^c Myo5a^d/Myo5a^d Hr^hr/Hr^hr
  
  albino, unaffected
  Related Genotype: Tyrp1^b/Tyrp1^b Tyr^c/Tyr^c Myo5a^d/Myo5a^d Hr^hr/+
Citation
When using the HRS/J mouse strain in a publication, please include JAX stock #000673 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous and Homozygous for HR, 1 pair minimum

Related Products and Services

Frozen Mouse Embryo	HRS/J Frozen Embryos	$2595.00
Frozen Mouse Embryo	HRS/J Frozen Embryos	$2595.00
Frozen Mouse Embryo	HRS/J Frozen Embryos	$3373.50
Frozen Mouse Embryo	HRS/J Frozen Embryos	$3373.50

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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. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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