Strain Name: |
HRS/J |
|---|---|
Stock Number: |
000673 |
Availability: | Repository-Cryopreserved |
Price and Supply Information | |
General Terms and Conditions |
| Former Name |
Hairless (Changed: 15-DEC-04
) |
| Genes & Alleles | Hr; Hrhr; Myo5a; Myo5ad; |
Product Information
Strain Details
Type Inbred Strain Additional information on Inbred Strains. Type JAX® GEMM® Strain - Mutant Strain Additional information on JAX® GEMM® Strains. Type JAX® GEMM® Strain - Spontaneous Mutation Species laboratory mouse H2 Haplotype k Generation F93 Appearance
unpigmented, without hair
Related Genotype: Tyrp1b/Tyrp1b Tyrc/Tyrc Myo5ad/Myo5ad Hrhr/Hrhr
albino, unaffected
Related Genotype: Tyrp1b/Tyrp1b Tyrc/Tyrc Myo5ad/Myo5ad Hrhr/+Strain 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).Strain Development
The hairless mutation (Hrhr) 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 (Tyrp1b), albino (Tyrc), dilute (Myo5ad) 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.
Related Disease (OMIM) Terms |
Mammalian Phenotype Terms assigned by genotype |
Gene & Allele Details
| Allele Symbol | Hrhr | ||
|---|---|---|---|
| Allele Name | hairless | ||
| Common Name(s) | hr; | ||
| Gene Symbol and Name | Hr, hairless | ||
| Chromosome | 14 | ||
| Gene Common Name(s) | ALUNC; AU; HSA277165; N; ba; baldy; bldy; rh; rh-bmh; rhino-bald Mill Hill; | ||
| General Note | Homozygous Hrhr/Hrhr mice develop a normal coat up to the age of about 10 days, but then lose all hair. The complete hair is lost from the follicle, not merely broken off. Waves of hair growth producing a few thin fuzzy hairs occur at intervals of about a month for some time thereafter, but the animals eventually appear continuously hairless (J:2409).The vibrissae are repeatedly regrown and shed, and become more abnormal with age. Toenails are excessively long and curved. There ishyperkeratosis of the stratified epithelium and upper part of the hair canals beginning at about 14 days. Hair club formation is abnormal, with the internal root sheath coalescing around the terminal part of the hair shaft so that the lower part of the external root sheath fails to follow the ascending hair club and becomes stranded in the dermis. Cysts develop from two sources, the hyperkeratotic upper part of the hair canals, and the sheaths of the abnormal follicles stranded in the dermis (J:14940, J:5239). Some cysts arise from isolated sebaceous glands. Regardless of their origin, all cysts undergo a sebaceous transformation and later a keratinization (J:14889).Hairless mice are generally fertile, but most females do not nurse their young well (J:2409).Homozygous hairless mice of the inbred HRS/J strain have a higher incidence of leukemia with earlier onset than their normal sibs, a 13-fold higher titer of ecotropic virus in tail extracts at 6 months of age (J:5726), a 100-fold higher titer of xenotropic virus in the thymus at 8 months of age (J:5908), and a lower cellular immune response to tumor viruses that may be responsible for the increased tumor susceptibility of the mice (J:6535). The incidence of leukemia in Hr homozygotes can be significantly reduced by passive immunization with virus-specific antiserum (J:6059). The lower cellular immune response of these mice is characteristic of spleen cells but not of lymph node cells and is due to a deficiency of T helper (Ly-1+) cells (J:6375, J:6087).The Hrhr mutation was caused by a retroviral integration, as shown by the complete concordance of the mutation and the provirus in several strains carrying Hr and the excision of the provirus in a haired revertant (J:9252). The gene mutated in hr has been identified and cloned. Its predicted protein product has 1182 amino acids, and includes a zinc finger domain. Expression sites are consonant with the sites of abnormalities in hairless mutants (J:19624). The Hrhr mutation disrupts the integrity of tissues in the hair follicle (J:47743). | ||
| Molecular Note | Mice homozygous for hr contain one or more MLV proviruses closely linked to this allele. Molecular analysis of an hr (haired) revertant showed the presence of only a single proviral, MX40, LTR establishing a causal relationship between the viral integration and the hr mutant allele. [MGI Ref ID J:92053] [MGI Ref ID J:9252] | ||
| Allele Symbol | Myo5ad | ||
| Allele Name | dilute | ||
| Common Name(s) | d; dv; maltese dilution; | ||
| Strain of Origin | old mutant of the mouse fancy | ||
| Gene Symbol and Name | Myo5a, myosin Va | ||
| Chromosome | 9 | ||
| Gene Common Name(s) | 9630007J19Rik; AI413174; AI661011; D; Dbv; Dop; GS1; MVa; MYH12; MYO5; MYR12; Myo5; MyoVA; RIKEN cDNA 9630007J19 gene; d; dilute; expressed sequence AI413174; expressed sequence AI661011; flail; flailer; flr; myosin V; nmf244; | ||
| General Note |
Mutations at the Myo5a locus lighten coat color through an abnormal morphology of melanocytes that causes uneven pigmentation of the hair shaft (J:11005). Most of these mutations also cause severe neurological defects; in some mutant forms, these defectslead to early death (J:12978), while in others life span is normal, but convulsions and loss of equilibrium occur after about four months of age (J:16915). Maltese dilution, as this mutation was originally called, is an old mutation of the mouse fancy. The blue-gray color of the hair produced by this mutation in nonagouti (a/a) mice is caused by clumping of the melanin pigment into a few large masses (J:12958). The melanocytes are misshapen, with fewer and thinner dendritic processes than wild-type melanocytes, and melanin granules are largely clumped around the nucleus (J:12970). Incorporation of tyrosine into melanin proceeds at a normal rate (J:12173), and the fine structure of the melanin granules is normal (J:5346). Cultured primary melanocytesfrom dilute homozygotes are normal in morphology but display clustering of melanosomes (J:37976). Griscelli disease (Chediak-Higashi-like syndrome, OMIM 214450) is a human autosomal recessive disorder whose symptoms include pigment dilution, immunodeficiency, and acute lethal lymphocyte and macrophage activation. Melanocyte malformation is characteristic of the pigment abnormality. The immunological abnormality includes absence of cutaneous hypersensitivity and impaired function of natural-killer cells. Griscelli disease resembles the dilute-lethal mouse mutant, except for the neurological disorder in the mouse. The locus for Griscelli disease colocalizes with the locus for myosin Va, which is mutated in at least some Griscelli patients. Griscelli disease is thus the homolog of mouse Maltese dilution (J:41253). The original Myo5ad mutation which identified the locuswas caused by insertion of an ecotropic murine leukemia virus (see Emv3) (J:6844, J:6587). All other mutations examined lack the virus. Reversions of Myo5ad to wild-type, which have been reported frequently, are caused by excision of the virusleaving exactly one long terminal repeat in place (J:7092). The virus is integrated into a noncoding region of the DNA (J:7751). | ||
Control Information
| Allele | Control | |
|---|---|---|
| Hrhr | Heterozygote from the colony | |
| Considerations for Choosing Controls | ||
| Control Pricing Information for JAX® GEMM® Strains | ||
Colony Maintenance
| Diet Information | LabDiet® 5K52/5K67 |
|---|
Related Strains
Strains carrying Hrhr allele
001737 B6.A-H2-T18a.HRS-Hrhr/J 002922 D2.HRS-Hrhr/J 001103 HRS/J-Hrhr Esdb/+ Esdb/J 002335 SKH2/J 000147 WLHR/LeJ View Strains carrying Hrhr (5 strains)
001005 AKXD1/TyJ 001003 AKXD11/TyJ 000765 AKXD13/TyJ 000779 AKXD14/TyJ 000954 AKXD15/TyJ 001093 AKXD18/TyJ 000776 AKXD2/TyJ 001062 AKXD21/TyJ 000947 AKXD22/TyJ 000949 AKXD25/TyJ 000764 AKXD27/TyJ 000959 AKXD3/TyJ 000285 B6.Cg-Rorasg + +/+ Myo5ad Bmp5se/J 000652 BDP/J 000036 BXD1/TyJ 000013 BXD16/TyJ 000015 BXD18/TyJ 000010 BXD19/TyJ 000077 BXD21/TyJ 000043 BXD22/TyJ 000081 BXD25/TyJ 006255 BXD25/TyJRwwJ 000029 BXD29/TyJ 000037 BXD5/TyJ 000007 BXD6/TyJ 000084 BXD8/TyJ 000105 BXD9/TyJ 000284 CWD/LeJ 000670 DBA/1J 000671 DBA/2J 000963 DBA/2J-Myo5ad+17J/Myo5ad/J 000964 DBA/2J-Myo5ad+18J/Myo5ad/J 000067 DBA/2J-Myo5ad+2J/Myo5ad/J 000674 I/LnJ 001850 MEV-Q/TyJ 001855 MEV-V/TyJ 003345 MEV/2Ty-Emv64/J 000679 P/J 000644 SEA/GnJ 000390 STOCK Myo5ad Ds/J 000994 STOCK a Myo5ad Mregdsu/J 000286 STOCK a/a Myo5ad fd/+ +/J
007621 B6.129S6-Hrtm1Cct/J 007622 B6;SJL-Tg(KRT14-Hr)551Cct/J 000758 C57BL/6J-Hbbp Hrrh-7J/J 000266 RHJ/Le 001591 RHJ/LeJ
005012 A.B6 Tyr+-Myo5ad-l31J/J 001013 B10.D2/nSnJ-Myo5ad-n/J 000502 B6 x B6CBCa Aw-J/A-Myo5aflr Gnb5flr/J 000963 DBA/2J-Myo5ad+17J/Myo5ad/J 000964 DBA/2J-Myo5ad+18J/Myo5ad/J 000067 DBA/2J-Myo5ad+2J/Myo5ad/J 000253 DLS/LeJ
Additional Web Information
Genetic Quality Control Annual Report
JAX® NOTES, January 1989; 436. Phenotypic abnormalities in hr-locus mutants.
JAX® NOTES, October 1988; 435. Introduction of Rhino (hrrh) into Jackson Laboratory Production Colonies.
JAX® NOTES, Spring 1990; 441. Imperforate Vagina and Mucometra in Mice.
Research Applications
This mouse can be used to support research in many areas including:Hrhr related
Myo5ad relatedCancer Research
Increased Tumor Incidence (Leukemia: lymphocytic)
Increased Tumor Incidence (Lymphomas: thymic)
Increased Tumor Incidence (Skin Cancers: Induced)
Toxicology
Cardiovascular Research
Diet-Induced Atherosclerosis (Relatively Resistant)
Dermatology Research
Skin and Hair Texture Defects
Immunology and Inflammation Research
Immunodeficiency Associated with Other Defects
Research Tools
Toxicology Research (drug/compound testing)
Dermatology Research
Color and White Spotting Defects
Mouse/Human Gene Homologs
Griscelli Syndrome
References
Additional ReferencesPrice and Supply Information
| Strain Name: | HRS/J |
| Stock Number: | 000673 |
Price Details
IMPORTANT NOTE: Prices are based on shipping destination. The shipping destinations are:
- USA, Canada and Mexico
- International
*Pricing for Shipping Destination selected:
International
| Price(s) in US dollars ($) | |||||
|---|---|---|---|---|---|
| Cryorecovery Fee | $2470.00 | ||||
Supply Details
| Standard Supply | Repository-Cryopreserved. Must Be Recovered. Please refer to pricing and supply notes for further information. |
|---|---|
| Supply Notes |
Cryorecovery - Standard. The recovery process begins when a signed agreement form is returned to the Customer Service Department after order placement. Although results vary by strain, at least two males and two females (two pairs) will be provided, typically within 15 weeks of our receipt of the signed agreement form. If the first recovery attempt is unsuccessful or only one pair is recovered, a second recovery will be done, extending the delivery time to approximately 25 weeks. At least one member of each pair will be of known genotype and will carry the mutation if it is a mutant strain. Please note that pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Price represents a repository maintenance fee, which includes the cost of recovery of the strain from the cryopreservation resource and the periodic replacement of the frozen embryos used for recovery. Cryorecovery to establish a Dedicated Supply for greater quantities of mice. |
| Licensing | See General Terms and Conditions below |
| Control Information | View Control Information in Strain Details. View Control Pricing Information for JAX® Strains. |
General Terms and Conditions
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The Jackson Laboratory's Genotype Promise
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.Ordering and Purchasing Information
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