Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Segregating Inbred; Type Mutant Strain; Additional information on Genetically Engineered and Mutant Mice. Type Inbred Strain; Additional information on Inbred Strains. Visit our online Nomenclature tutorial. Species laboratory mouse Generation F83p

Appearance
brown, haired, normal gait
Related Genotype: a/a Tyrp1^b/Tyrp1^b wl + Esd^c/+ Hr^hr Esd^c or a/a Tyrp1^b/Tyrp1^b ? + Esd^c/+ ? Esd^c

brown, haired, wobbly gait
Related Genotype: a/a Tyrp1^b/Tyrp1^b + wl Esd^c/? wl Esd^c

pigmented, hairless, normal gait
Related Genotype: a/a Tyrp1^b/Tyrp1^b Hr^hr + Esd^c/Hr^hr ? Esd^c

Important Note
This strain is homozygous for Esd^c and segregating for Hr^hr and wl, which are held in repulsion.

Description
WLHR/Le is a balanced stock with wabbler-lethal (wl) and hairless (hr) spontaneous mutations maintained in repulsion on Chromosome 14. Homozygous wabbler-lethal mutant mice are first recognizable at 12 days of age and usually die at about four weeks. They have an abnormal wobbly gait and a pronounced tremor when walking. In an extensive study of behavioral development of this mutant, homozygous wabbler-lethal mice were shown to be deficient in nearly all behaviors tested. Histological examination showed myelin degeneration widely distributed throughout the CNS, particularly in the vestibulocerebellar and spinocerebellar systems. Electron microscopy showed widespread axonal (Wallerian) degeneration in the medulla with secondary myelin dissolution. Similar abnormalities were present to a lesser extent in the basal ganglia, spinal cord, and cerebellum and in the optic nerve. Homozygous hairless mutant mice have a higher incidence and earlier onset of leukemia, reducible by virus-specific antibody. A deficiency of splenic T helper cells (Ly1⁺) may account for low cellular immune response of homozygous mutant mice. The coat is normal on hairless 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 statified 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.

Development
The first wabbler lethal (wl) mouse appeared in descendents of a non-inbred pirouette (pi/pi) mouse carrying brown (Typr1^b) and nonagouti (a) that was returned to the Jackson Laboratory from Dr. R. A. Fisher in 1948 after the fire. The pirouette male was mated to a C57BL/6J female and several lines were made. An outcross was also made to strain HD/Hu of Dr. Katrina Hummel. Strain HD/Hu was homozygous for hairless (Hr^hr) and dilute (Myo5a^d). The stock was bred using tested but non-sibling matings until 1958 when inbreeding was started as a balanced stock with wl and hr in repulsion phase because they were closely linked on chromosome 14. The stock was also selected to be homozygous brown and nonagouti. It was cryopreserved in 1989 by mating known doubly heterozygous males to either known heterozygous or untested females at generations F115-120.

Related Strains

Strains carrying   Hr^hr allele

001737	B6.A-H2-T18a.HRS-Hrhr/J
002922	D2.HRS-Hrhr/J
000673	HRS/J
001103	HRS/J-Hrhr Esdb/+ Esdb/J
002335	SKH2/J

View Strains carrying   Hr^hr     (5 strains)

Strains carrying   wl allele

004835

B6 x B6JCu.Cg-wl/J

View Strains carrying   wl     (1 strain)

Strains carrying other alleles of Esd

001425	A/J-Esdc-mJ/J
001103	HRS/J-Hrhr Esdb/+ Esdb/J
000790	LT.MOL-Esdc/J

View Strains carrying other alleles of Esd     (3 strains)

Strains carrying other alleles of Hr

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

View Strains carrying other alleles of Hr     (5 strains)

Strains carrying other alleles of wl

001767	C3H/HeSnJ-wlvmd/J
002457	CBA/J-wl3J/J

View Strains carrying other alleles of wl     (2 strains)

Additional Web Information

JAX^® NOTES, January 1989; 436. Phenotypic abnormalities in hr-locus mutants.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms

	Alopecia Universalis Congenita; ALUNC - Models with phenotypic similarity to human disease where etiologies involve orthologs.1
	Atrichia with Papular Lesions; APL - Models with phenotypic similarity to human disease where etiologies involve orthologs.1

1 Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

View Mammalian Phenotype Terms

Mammalian Phenotype Terms

      assigned by genotype

The following phenotype information may relate to a genetic background differing from this JAX^® Mice strain.

Hr^hr/Hr^hr

        Background Not Specified

• skin/coat/nails phenotype
• abnormal skin morphology (MGI Ref ID J:2409)
  • thickened cutis
• abnormal dermis reticular layer morphology (MGI Ref ID J:2409)
  • cystic
• dermal cysts (MGI Ref ID J:14889)
• epidermal hyperplasia (MGI Ref ID J:14940)
• hyperkeratosis (MGI Ref ID J:14940)
• alopecia (MGI Ref ID J:2409)
  • beginning ~15 days of age and progressing from nose back
• deformed nails (MGI Ref ID J:2409)
  • curved
• endocrine/exocrine gland phenotype
• abnormal mammary gland morphology (MGI Ref ID J:2409)
  • small
  • nipple at bottom of cup-shaped depression in skin
  • no ducts
• sebaceous gland atrophy (MGI Ref ID J:2409)
• reproductive system phenotype
• abnormal mammary gland morphology (MGI Ref ID J:2409)
  • small
  • nipple at bottom of cup-shaped depression in skin
  • no ducts
• behavior/neurological phenotype
• abnormal nursing (MGI Ref ID J:2409)
  • failure

Hr^hr/Hr^hr

        HRS/J

• hearing/vestibular/ear phenotype
• absent linear vestibular evoked potential (MGI Ref ID J:116914)
  • VESPs are absent at the maximum stimulus intensity used
• tumorigenesis
• leukemia (MGI Ref ID J:5726)
  • increased incidence
  • increased 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
• hematopoietic system phenotype
• decreased T cell number (MGI Ref ID J:6087)
  • of CD5+ T cells
• decreased T cell proliferation (MGI Ref ID J:6375)
  • to alloantigens by T helper cells
• increased macrophage cell number (MGI Ref ID J:150402)
  • 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 (MGI Ref ID J:6087)
  • of CD5+ T cells
• decreased T cell proliferation (MGI Ref ID J:6375)
  • to alloantigens by T helper cells
• increased macrophage cell number (MGI Ref ID J:150402)
  • 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

wl/wl

        Background Not Specified

• nervous system phenotype
• *normal* nervous system phenotype (MGI Ref ID J:13068)
  • demyelination is not found in the telencephalon at 2.5 weeks of age
  • there is no myelin degeneration detected in the thalamus
• demyelination (MGI Ref ID J:13068)
  • at one week of age a small amount of myelin degeneration can be found in the ventral funiculus of the spinal cord; at two weeks of age myelin degeneration is marked in the vestibulo-spinal tracts and beginning in the spino-cerebellar tracts; and by 2.5 weeks of age very severe demyelination is found throughout the archi- and paleocerebellar systems, with heavy degeneration permeating the vestibulo-spinal tract, dorsal spinocerebellar tract, brachium conjunctivum, magnocellular red nucleus, rubrospinal tract, vestibular nerve and nuclei, juxtarestiform body, trapezoid body and the superior olivary nucleus, and moderate degeneration in the medial lemnicus, medial longitudinal fasiculus and tecto-spinal tracts
  • in the vestibulosponal tract from the lateral vestibular nucleus to the spinal cord, and in the entering fibers of the eighth cranial nerve, the juxtaresiform body, the medullary center of the cerebellum, the medial longitudinal fasciculus, the trapezoid body, the lateral lemniscus, brachium conjunctivum, red nucleus, and the rubrospinal and tectospinal tracts
• lethality-postnatal
• lethality at weaning (MGI Ref ID J:13068)
  • most homozygotes die by wean age, with males dying at approximately 3 weeks of age and females dying approximately a week later
• behavior/neurological phenotype
• *normal* behavior/neurological phenotype (MGI Ref ID J:13068)
  • can orient in water and swim
• abnormal gait (MGI Ref ID J:13068)
• abnormal motor coordination/ balance (MGI Ref ID J:15162)
  • swaying of the body, dragging of the hind limbs and progressive incoordination of the limbs when walking
• ataxia (MGI Ref ID J:15162)
  • homozygotes have difficulty in walking and when trying to walk seem to pull the hind feet along rather than pushing off with them
• impaired limb coordination (MGI Ref ID J:15162)
• abnormal reflex (MGI Ref ID J:13068)
  • no reaction to pinching of the tail
• limb grasping (MGI Ref ID J:13068)
  • when homozyogtes are lifted by the tail, the hind feet lock together in a spasm
• tremors (MGI Ref ID J:13068)
• hearing/vestibular/ear phenotype
• *normal* hearing/vestibular/ear phenotype (MGI Ref ID J:15162)
  • normal hearing and auditory reflexes
• homeostasis/metabolism phenotype
• abnormal circulating amino acid level (MGI Ref ID J:5108)
  • plasma phenylalanine concentration rises after 18 days of age to abnormally high levels and phenylalanine loading experiments show that at 22 days of age homozygotes can not normally metabolize exogenous phenylalanine, although they can at 14 days of age
  • plasma tyrosine concentration is higher than normal at 14 days of age then rapidly drops to abnormally low levels (at 26 days of age 13.36 ug/ml vs 23.12 ug/ml in heterozygotes) and plasma tryptophan levels are lower than normal at 14 days of age and become progressively lower to 26 days of age (14.13 ug/ml vs 22.18 ug/ml in heterozygotes), although loading experiments show that homozygotes handle added tyrosine and tryptophan in a manner comparable to that of heterozygous littermates
• abnormal enzyme/ coenzyme level (MGI Ref ID J:5108)
  • liver homogenates have decreased phenylalanine hydroxylase activity, decreased phenylalanine-sodium pyruvate transaminase activity, and increased phenylalanine-alpha-ketoglutarate transaminase activity, increased tyrosine-alpha-ketoglutarate transaminase activity, increased tryptophan-alpha-ketoglutarate activity, and increased tryptophan pyrrolase activity
• hypoglycemia (MGI Ref ID J:14851)
  • mice are hypoglycemic from 20 days until death

wl/wl

        involves: C57BL/6J

• nervous system phenotype
• optic nerve degeneration (MGI Ref ID J:2856)
  • at 28 days of age there is primary axonal degeneration of the optic nerve, but significant dysmyelination or hypomyelination are not found in the optic nerves at this timepoint
• vision/eye phenotype
• optic nerve degeneration (MGI Ref ID J:2856)
  • at 28 days of age there is primary axonal degeneration of the optic nerve, but significant dysmyelination or hypomyelination are not found in the optic nerves at this timepoint
• growth/size phenotype
• decreased body weight (MGI Ref ID J:2856)
  • at 28 days of age the average weight of males, 6.3g, is less than half that of normal controls, 14.2g

wl/wl⁺

        Background Not Specified

• behavior/neurological phenotype
• abnormal motor coordination/ balance (MGI Ref ID J:13068)
  • symptoms are subtle and obvious only to experienced observers
  • all heterozygotes are not symptomatic
• ataxia (MGI Ref ID J:13068)
  • mild ataxia is characterized by the hind feet going out to the side more than normal and the body being closer to the ground
  • heterozygous mice are distinguishable from normal mice only in exceptional cases
• nervous system phenotype
• demyelination (MGI Ref ID J:13068)
  • at 2 weeks of age a small amount of myelin degeneration is found in the vestibulo-spinal tract and at 2.5 weeks myelin degeneration is still confined to the vestibulo-spinal pathway with the cerebellar systems unaffected
  • moderate demyelination restricted to the vestibulospinal tract

View Research Applications

Research Applications

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

Metabolism Research

Hr^hr related

Cancer Research
Increased Tumor Incidence
      Leukemia: lymphocytic
      Lymphomas: thymic
      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

wl related

Neurobiology Research
Ataxia (Movement) Defects
Myelination Defects
Tremor Defects
Vestibular and Hearing Defects

Sensorineural Research
Vestibular and Hearing Defects

Genes & Alleles

Gene & Allele Information

Allele Symbol		Hrhr
Allele Name		hairless
Allele Type		Spontaneous
Common Name(s)		hr;
Gene Symbol and Name		Hr, hairless
Chromosome		14
Gene Common Name(s)		ALUNC; AU; FLJ98880; HSA277165; MUHH; MUHH1; N; ba; baldy; bldy; rh; rh-bmh; rhino-bald Mill Hill;
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. [MGI Ref ID J:19624] [MGI Ref ID J:92053] [MGI Ref ID J:9252]
Allele Symbol		wl
Allele Name		wabbler lethal
Allele Type		Spontaneous
Common Name(s)		Wl;
Strain of Origin		STOCK pi
Gene Symbol and Name		wl, wabbler-lethal
Chromosome		14
Gene Common Name(s)		vestibulomotor degeneration; vmd;
Molecular Note		A heterozygous effect is observed in the presence of unspecified genetic modifiers.
Gene Symbol and Name		Esd, esterase D/formylglutathione hydrolase
Chromosome		14
Gene Common Name(s)		Es-10; Es10; FGH; FLJ11763; esterase 10; esterase D;

Genotyping

Genotyping Information

This strain will not have a genotyping protocol or one is not currently available.

Helpful Links

Genotyping resources and troubleshooting

References

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):7717-21. [PubMed: 8052649]  [MGI Ref ID 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):1558-62. [PubMed: 6447727]  [MGI Ref ID J:6375]

Reske-Kunz AB; Scheid MP; Boyse EA. 1979. Disproportion in T-cell subpopulations in immunodeficient mutant hr/hr mice. J Exp Med 149(1):228-33. [PubMed: 310859]  [MGI Ref ID J:6087]

Hr^hr related

Aberg KM; Man MQ; Gallo RL; Ganz T; Crumrine D; Brown BE; Choi EH; Kim DK; Schroder JM; Feingold KR; Elias PM. 2008. Co-regulation and interdependence of the mammalian epidermal permeability and antimicrobial barriers. J Invest Dermatol 128(4):917-25. [PubMed: 17943185]  [MGI Ref ID J:135506]

Ahmad W; Panteleyev AA; Christiano AM. 1999. The molecular basis of congenital atrichia in humans and mice: mutations in the hairless gene. J Investig Dermatol Symp Proc 4(3):240-3. [PubMed: 10674375]  [MGI Ref ID J:59939]

Astner S; Wu A; Chen J; Philips N; Rius-Diaz F; Parrado C; Mihm MC; Goukassian DA; Pathak MA; Gonzalez S. 2007. Dietary lutein/zeaxanthin partially reduces photoaging and photocarcinogenesis in chronically UVB-irradiated Skh-1 hairless mice. Skin Pharmacol Physiol 20(6):283-91. [PubMed: 17717424]  [MGI Ref ID J:128747]

Balansky RM; Izzotti A; D'Agostini F; Camoirano A; Bagnasco M; Lubet RA; De Flora S. 2003. Systemic genotoxic effects produced by light, and synergism with cigarette smoke in the respiratory tract of hairless mice. Carcinogenesis 24(9):1525-32. [PubMed: 12844483]  [MGI Ref ID J:85507]

Brooke HC. 1926. Hairless mice J Hered 17:173-74.  [MGI Ref ID J:2405]

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):7717-21. [PubMed: 8052649]  [MGI Ref ID J:19624]

Cachon-Gonzalez MB; San-Jose I; Cano A; Vega JA; Garcia N; Freeman T; Schimmang T; Stoye JP. 1999. The hairless gene of the mouse: relationship of phenotypic effects with expression profile and genotype. Dev Dyn 216(2):113-26. [PubMed: 10536052]  [MGI Ref ID J:57947]

Clark EA; Shultz LD; Pollack SB. 1981. Mutations in mice that influence natural killer (NK) cell activity. Immunogenetics 12(5-6):601-13. [PubMed: 6971254]  [MGI Ref ID J:6485]

Crew FAE; Mirskaia L. 1931. The character of "hairless" in the mouse J Genet 25:17-24.  [MGI Ref ID J:2409]

DERINGER MK. 1956. The effect of subcutaneous inoculation of 4-o-tolylazo-o-toluidine in strain HR mice. J Natl Cancer Inst 17(4):533-9. [PubMed: 13367821]  [MGI Ref ID J:24688]

Doig J; Anderson C; Lawrence NJ; Selfridge J; Brownstein DG; Melton DW. 2006. Mice with skin-specific DNA repair gene (Ercc1) inactivation are hypersensitive to ultraviolet irradiation-induced skin cancer and show more rapid actinic progression. Oncogene 25(47):6229-38. [PubMed: 16682947]  [MGI Ref ID J:115849]

Dunn TB; Deringer MK. 1968. Reticulum cell neoplasm, type B, or the Hodgkin's-like lesion of the mouse. J Natl Cancer Inst 40(4):771-821. [PubMed: 4869134]  [MGI Ref ID J:2417]

Dwivedi C; Valluri HB; Guan X; Agarwal R. 2006. Chemopreventive effects of alpha-santalol on ultraviolet B radiation-induced skin tumor development in SKH-1 hairless mice. Carcinogenesis 27(9):1917-22. [PubMed: 16679309]  [MGI Ref ID J:113353]

Egberts F; Heinrich M; Jensen JM; Winoto-Morbach S; Pfeiffer S; Wickel M; Schunck M; Steude J; Saftig P; Proksch E; Schutze S. 2004. Cathepsin D is involved in the regulation of transglutaminase 1 and epidermal differentiation. J Cell Sci 117(Pt 11):2295-307. [PubMed: 15126630]  [MGI Ref ID J:89747]

Elias PM; Arbiser J; Brown BE; Rossiter H; Man MQ; Cerimele F; Crumrine D; Gunathilake R; Choi EH; Uchida Y; Tschachler E; Feingold KR. 2008. Epidermal vascular endothelial growth factor production is required for permeability barrier homeostasis, dermal angiogenesis, and the development of epidermal hyperplasia: implications for the pathogenesis of psoriasis. Am J Pathol 173(3):689-99. [PubMed: 18688025]  [MGI Ref ID J:139588]

Fischer SM; Pavone A; Mikulec C; Langenbach R; Rundhaug JE. 2007. Cyclooxygenase-2 expression is critical for chronic UV-induced murine skin carcinogenesis. Mol Carcinog 46(5):363-71. [PubMed: 17219415]  [MGI Ref ID J:121635]

Fraser FC. 1946. The expression and interaction of hereditary factors producing hypotrichosis in the mouse: histology and experimental results. Can J Res 24:10-25.  [MGI Ref ID J:14940]

Gallagher CH; Canfield PJ; Greenoak GE; Reeve VE. 1984. Characterization and histogenesis of tumors in the hairless mouse produced by low-dosage incremental ultraviolet radiation. J Invest Dermatol 83(3):169-74. [PubMed: 6470519]  [MGI Ref ID J:127204]

Gates AH; Arundell FD; Karasek MA. 1969. Hereditary defect of the pilosebaceous unit in a new double mutant mouse. J Invest Dermatol 52(2):115-8. [PubMed: 5774889]  [MGI Ref ID J:126589]

Hachem JP; Houben E; Crumrine D; Man MQ; Schurer N; Roelandt T; Choi EH; Uchida Y; Brown BE; Feingold KR; Elias PM. 2006. Serine Protease Signaling of Epidermal Permeability Barrier Homeostasis. J Invest Dermatol 126(9):2074-2086. [PubMed: 16691196]  [MGI Ref ID J:111734]

Halin C; Fahrngruber H; Meingassner JG; Bold G; Littlewood-Evans A; Stuetz A; Detmar M. 2008. Inhibition of chronic and acute skin inflammation by treatment with a vascular endothelial growth factor receptor tyrosine kinase inhibitor. Am J Pathol 173(1):265-77. [PubMed: 18535184]  [MGI Ref ID J:137380]

Heiniger HJ; Huebner RJ; Meier H. 1976. Effect of allelic substitutions at the hairless locus on endogenous ecotropic murine leukemia virus titers and leukemogenesis. J Natl Cancer Inst 56(5):1073-4. [PubMed: 186616]  [MGI Ref ID J:5726]

Heiniger HJ; Meier H; Kaliss N; Cherry M; Chen HW; Stoner RD. 1974. Hereditary immunodeficiency and leukemogenesis in HRS-J mice. Cancer Res 34(1):201-11. [PubMed: 4588546]  [MGI Ref ID J:24605]

Heston WE. 1963. Genetics of Neoplasia. In: Methodology in Mammalian Genetics. Holden-Day, San Francisco.  [MGI Ref ID J:23470]

Hiai H; Morrissey P; Khiroya R; Schwartz RS. 1977. Selective expression of xenotropic virus in congenic HRS/J (hairless) mice. Nature 270(5634):247-9. [PubMed: 201855]  [MGI Ref ID J:5908]

Jensen JM; Schutze S; Forl M; Kronke M; Proksch E. 1999. Roles for tumor necrosis factor receptor p55 and sphingomyelinase in repairing the cutaneous permeability barrier. J Clin Invest 104(12):1761-70. [PubMed: 10606630]  [MGI Ref ID J:59056]

Jeong SK; Kim HJ; Youm JK; Ahn SK; Choi EH; Sohn MH; Kim KE; Hong JH; Shin DM; Lee SH. 2008. Mite and cockroach allergens activate protease-activated receptor 2 and delay epidermal permeability barrier recovery. J Invest Dermatol 128(8):1930-9. [PubMed: 18305573]  [MGI Ref ID J:141618]

Johnson DA; Meier H. 1981. Immune responsiveness of HRS/J mice to syngeneic lymphoma cells. J Immunol 127(2):461-4. [PubMed: 6265551]  [MGI Ref ID J:6535]

Jones SM; Johnson KR; Yu H; Erway LC; Alagramam KN; Pollak N; Jones TA. 2005. A quantitative survey of gravity receptor function in mutant mouse strains. J Assoc Res Otolaryngol 6(4):297-310. [PubMed: 16235133]  [MGI Ref ID J:116914]

Kajiya K; Hirakawa S; Detmar M. 2006. Vascular endothelial growth factor-A mediates ultraviolet B-induced impairment of lymphatic vessel function. Am J Pathol 169(4):1496-503. [PubMed: 17003502]  [MGI Ref ID J:113381]

Kato M; Ohgami N; Kawamoto Y; Tsuzuki T; Hossain K; Yanagishita T; Ohshima Y; Tsuboi H; Yamanoshita O; Matsumoto Y; Takahashi M; Nakashima I. 2007. Protective effect of hyperpigmented skin on UV-mediated cutaneous cancer development. J Invest Dermatol 127(5):1244-9. [PubMed: 17159911]  [MGI Ref ID J:121091]

Kato M; Takeda K; Kawamoto Y; Tsuzuki T; Kato Y; Ohno T; Hossain K; Iftakhar-E-Khuda I; Ohgami N; Isobe K; Takahashi M; Nakashima I. 2006. Novel Hairless RET-Transgenic Mouse Line with Melanocytic Nevi and Anagen Hair Follicles. J Invest Dermatol 126(11):2547-50. [PubMed: 16778787]  [MGI Ref ID J:113399]

Kaya G; Tran C; Sorg O; Hotz R; Grand D; Carraux P; Didierjean L; Stamenkovic I; Saurat JH. 2006. Hyaluronate fragments reverse skin atrophy by a CD44-dependent mechanism. PLoS Med 3(12):e493. [PubMed: 17177600]  [MGI Ref ID J:134166]

Keeler CE. 1931. The Independence of Dominant Spotting and Recessive Spotting ('Piebald') in the House Mouse. Proc Natl Acad Sci U S A 17(2):101-2. [PubMed: 16587618]  [MGI Ref ID J:153352]

Kimura Y; Sumiyoshi M. 2009. Olive leaf extract and its main component oleuropein prevent chronic ultraviolet B radiation-induced skin damage and carcinogenesis in hairless mice. J Nutr 139(11):2079-86. [PubMed: 19776181]  [MGI Ref ID J:153732]

Kinley JS; Moan J; Dall'Aqua F; Young AR. 1994. Quantitative assessment of epidermal melanogenesis in C3H/Tif hr/hr mice treated with topical furocoumarins and UVA radiation. J Invest Dermatol 103(1):97-103. [PubMed: 8027588]  [MGI Ref ID J:19313]

Kondo T; Shiomoto Y; Kondo T; and Kubo S. 1997. The "NOA" MOUSE; A NEW HAIR-DEFICIENT MUTANT (A POSSIBLE ANIMAL MODEL OF ALLERGIC DERMATITIS) Mouse Genome 95(3):698-700.  [MGI Ref ID J:43274]

MONTAGNA W; CHASE HB; MELARAGNO HP. 1952. The skin of hairless mice. I. The formation of cysts and the distribution of lipids. J Invest Dermatol 19(1):83-94. [PubMed: 14946445]  [MGI Ref ID J:14889]

Mann SJ. 1971. Hair loss and cyst formation in hairless and rhino mutant mice. Anat Rec 170(4):485-99. [PubMed: 5118596]  [MGI Ref ID J:5239]

Meier H; Myers DD; Huebner RJ. 1969. Genetic control by the hr-locus of susceptibility and resistance to leukemia. Proc Natl Acad Sci U S A 63(3):759-66. [PubMed: 4310515]  [MGI Ref ID J:24786]

Michna L; Wagner GC; Lou YR; Xie JG; Peng QY; Lin Y; Carlson K; Shih WJ; Conney AH; Lu YP. 2006. Inhibitory effects of voluntary running wheel exercise on UVB-induced skin carcinogenesis in SKH-1 mice. Carcinogenesis 27(10):2108-15. [PubMed: 16699173]  [MGI Ref ID J:113354]

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):1558-62. [PubMed: 6447727]  [MGI Ref ID J:6375]

Mucenski ML; Bedigian HG; Shull MM; Copeland NG; Jenkins NA. 1988. Comparative molecular genetic analysis of lymphomas from six inbred mouse strains. J Virol 62(3):839-46. [PubMed: 2828679]  [MGI Ref ID J:25442]

Murphy ED. 1966. Characteristic Tumors. In: Biology of the Laboratory Mouse. McGraw-Hill, New York.  [MGI Ref ID J:24830]

Panteleyev AA; Botchkareva NV; Sundberg JP; Christiano AM; Paus R. 1999. The role of the hairless (hr) gene in the regulation of hair follicle catagen transformation. Am J Pathol 155(1):159-71. [PubMed: 10393848]  [MGI Ref ID J:56076]

Panteleyev AA; van der Veen C; Rosenbach T; Muller-Rover S; Sokolov VE ; Paus R. 1998. Towards defining the pathogenesis of the hairless phenotype. J Invest Dermatol 110(6):902-7. [PubMed: 9620297]  [MGI Ref ID J:47743]

Pauling L. 1991. Effect of ascorbic acid on incidence of spontaneous mammary tumors and UV-light-induced skin tumors in mice. Am J Clin Nutr 54(6 Suppl):1252S-1255S. [PubMed: 1962578]  [MGI Ref ID J:634]

Pirinen E; Kuulasmaa T; Pietila M; Heikkinen S; Tusa M; Itkonen P; Boman S; Skommer J; Virkamaki A; Hohtola E; Kettunen M; Fatrai S; Kansanen E; Koota S; Niiranen K; Parkkinen J; Levonen AL; Yla-Herttuala S; Hiltunen JK; Alhonen L; Smith U; Janne J; Laakso M. 2007. Enhanced polyamine catabolism alters homeostatic control of white adipose tissue mass, energy expenditure, and glucose metabolism. Mol Cell Biol 27(13):4953-67. [PubMed: 17485446]  [MGI Ref ID J:122759]

Pottathil R; Meier H; Huebner RJ. 1978. Suppression of leukemogenesis in hairless mice by anti-type C viral immune gamma globulins. Naturwissenschaften 65(8):443-4. [PubMed: 213736]  [MGI Ref ID J:6059]

Reske-Kunz AB; Scheid MP; Boyse EA. 1979. Disproportion in T-cell subpopulations in immunodeficient mutant hr/hr mice. J Exp Med 149(1):228-33. [PubMed: 310859]  [MGI Ref ID J:6087]

Roelandt T; Giddelo C; Heughebaert C; Denecker G; Hupe M; Crumrine D; Kusuma A; Haftek M; Roseeuw D; Declercq W; Feingold KR; Elias PM; Hachem JP. 2009. The 'caveolae brake hypothesis' and the epidermal barrier. J Invest Dermatol 129(4):927-36. [PubMed: 19005485]  [MGI Ref ID J:150227]

Sato J; Yanai M; Hirao T; Denda M. 2000. Water content and thickness of the stratum corneum contribute to skin surface morphology. Arch Dermatol Res 292(8):412-7. [PubMed: 10994776]  [MGI Ref ID J:116955]

Sitaru C; Chiriac MT; Mihai S; Buning J; Gebert A; Ishiko A; Zillikens D. 2006. Induction of complement-fixing autoantibodies against type VII collagen results in subepidermal blistering in mice. J Immunol 177(5):3461-8. [PubMed: 16920988]  [MGI Ref ID J:139521]

Staats J. 1985. Standardized Nomenclature for Inbred Strains of Mice: eighth listing. Cancer Res 45(3):945-77. [PubMed: 3971387]  [MGI Ref ID J:50296]

Starcher B; O'Neal P; Granstein RD; Beissert S. 1996. Inhibition of neutrophil elastase suppresses the development of skin tumors in hairless mice. J Invest Dermatol 107(2):159-63. [PubMed: 8757756]  [MGI Ref ID J:34446]

Stoye JP; Fenner S; Greenoak GE; Moran C; Coffin JM. 1988. Role of endogenous retroviruses as mutagens: the hairless mutation of mice. Cell 54(3):383-91. [PubMed: 2840205]  [MGI Ref ID J:9252]

Sundberg JP (ed.). 1994. . In: Handbook of Mouse Mutations with Skin and Hair Abnormalities: Animal Models and Biomedical Tools. CRC Press, Boca Raton.  [MGI Ref ID J:30359]

Sundberg JP; Sundberg BA; Beamer WG. 1997. Comparison of chemical carcinogen skin tumor induction efficacy in inbred, mutant, and hybrid strains of mice: Morphologic variations of induced tumors and absence of a papillomavirus cocarcinogen. Mol Carcinog 20(1):19-32. [PubMed: 9328433]  [MGI Ref ID J:43880]

Suzu S; Tanaka-Douzono M; Nomaguchi K; Yamada M; Hayasawa H; Kimura F; Motoyoshi K. 2000. p56(dok-2) as a cytokine-inducible inhibitor of cell proliferation and signal transduction. EMBO J 19(19):5114-22. [PubMed: 11013214]  [MGI Ref ID J:150402]

Tober KL; Thomas-Ahner JM; Kusewitt DF; Oberyszyn TM. 2007. Effects of UVB on E prostanoid receptor expression in murine skin. J Invest Dermatol 127(1):214-21. [PubMed: 16917495]  [MGI Ref ID J:116974]

Tsukahara K; Kakuo S; Moriwaki S; Hotta M; Ohuchi A; Kitahara T; Harada N. 2008. The characteristics of aromatase deficient hairless mice indicate important roles of extragonadal estrogen in the skin. J Steroid Biochem Mol Biol 108(1-2):82-90. [PubMed: 17951050]  [MGI Ref ID J:130515]

Vollmar B; Morgenthaler M; Amon M; Menger MD. 2000. Skin microvascular adaptations during maturation and aging of hairless mice Am J Physiol Heart Circ Physiol 279(4):H1591-9. [PubMed: 11009445]  [MGI Ref ID J:65226]

Wang XP; Schunck M; Kallen KJ; Neumann C; Trautwein C; Rose-John S; Proksch E. 2004. The interleukin-6 cytokine system regulates epidermal permeability barrier homeostasis. J Invest Dermatol 123(1):124-31. [PubMed: 15191552]  [MGI Ref ID J:90509]

Wilgus TA; Koki AT; Zweifel BS; Rubal PA; Oberyszyn TM. 2003. Chemotherapeutic efficacy of topical celecoxib in a murine model of ultraviolet light B-induced skin cancer. Mol Carcinog 38(1):33-9. [PubMed: 12949841]  [MGI Ref ID J:85679]

Wulff BC; Kusewitt DF; VanBuskirk AM; Thomas-Ahner JM; Duncan FJ; Oberyszyn TM. 2008. Sirolimus reduces the incidence and progression of UVB-induced skin cancer in SKH mice even with co-administration of cyclosporine A. J Invest Dermatol 128(10):2467-73. [PubMed: 18463679]  [MGI Ref ID J:139918]

Zarach JM; Beaudoin GM rd; Coulombe PA; Thompson CC. 2004. The co-repressor hairless has a role in epithelial cell differentiation in the skin. Development 131(17):4189-200. [PubMed: 15280217]  [MGI Ref ID J:92053]

Zhang W; Hanks AN; Boucher K; Florell SR; Allen SM; Alexander A; Brash DE; Grossman D. 2005. UVB-induced apoptosis drives clonal expansion during skin tumor development. Carcinogenesis 26(1):249-57. [PubMed: 15498793]  [MGI Ref ID J:95011]

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wl related

Carroll EW; Curtis RL; Sullivan DA; Melvin JL. 1992. Wallerian degeneration in the optic nerve of the wabbler-lethal (wl/wl) mouse. Brain Res Bull 29(3-4):411-8. [PubMed: 1382814]  [MGI Ref ID J:2856]

Dickie MM; Schneider J; Harman PJ. 1952. A juvenile wabbler-lethal in the house mouse. J Hered 43:283-286.  [MGI Ref ID J:13068]

Harman PJ. 1954. Genetically controlled demyelination in the mammalian central nervous system Ann N Y Acad Sci 58:546-50.  [MGI Ref ID J:15162]

Lane PW; Dickie MM. 1961. Linkage of wabbler-lethal and hairless in the mouse J Hered 52:159-60.  [MGI Ref ID J:270]

Luse SA; Chenard C; Finke EH. 1967. The wabbler-lethal mouse. An electron microscopic study of the nervous system. Arch Neurol 17(2):153-61. [PubMed: 6028244]  [MGI Ref ID J:5028]

Murad S; Kishimoto Y. 1975. Alpha hydroxylation of lignoceric acid to cerebronic acid during brain development. Diminished hydroxylase activity in myelin-deficient mouse mutants. J Biol Chem 250(15):5841-6. [PubMed: 1150661]  [MGI Ref ID J:106960]

Siegel SJ; Rauch H. 1969. Aromatic amino acid metabolism in the wabbler-lethal mouse. Biochem Genet 2(4):311-8. [PubMed: 4388883]  [MGI Ref ID J:5108]

Thiessen DD. 1965. The wabbler-lethal mouse: a study in development Anim Behav 13:87-100.  [MGI Ref ID J:14851]

Health & husbandry

Health & Colony Maintenance Information

Currently there no information available for this strain. This may be due to the supply level of this strain.

Purchasing information

Pricing, Supply Level & Notes, Controls, General Terms & Conditions

Pricing

Supply Details

Standard Supply	Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
Supply Notes	Cryorecovery of Strains Needing Progeny Testing. At least two untested males and two untested females (two pairs) will be recovered (eight or more mice is typical). The total number of animals provided, their gender and genotype will vary. Untested animals typically are available to ship between 13 and 16 weeks from the date of your order. If the first recovery attempt is unsuccessful, a second recovery will be done, extending the overall recovery time to approximately 25 weeks. Progeny testing is required to identify the genotype of mice of this strain, as a genotyping assay is not available. This type of testing involves breeding the recovered animals and assessing the phenotype of the offspring in order to identify animals carrying the mutation of interest. We can perform the progeny testing for you as a service or we can ship all recovered animals to you for progeny testing at your facility. If you perform the progeny testing, there is NO guarantee that a carrier will be identified. If we perform progeny testing as a service, additional breeding time will be required. In this case, when a male and female (one pair) are identified that carry the mutation, they and their offspring will be shipped. Delivery time for strains requiring progeny testing often exceeds 25 weeks and may take 12 months or more due to the difficulties in breeding some strains. The progeny testing cost is in addition to the recovery cost and is based on the number of boxes used and the time taken to produce the mice identified as carrying the mutation. Please note that identified 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. Please contact Customer Service for more information on the cost of progeny testing for a strain: Tel: 1-800-422-6423 (from U.S.A., Canada and Puerto Rico only) or 1-207-288-5845 (from any location). The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary. Cryorecovery to establish a Dedicated Supply for greater quantities of mice. Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location). This strain is included in the Mouse Mutant Resource collection. Genomic DNA is available for this strain from the Mouse DNA Resource.
Important Note
This strain is homozygous for Esdc and segregating for Hrhr and wl, which are held in repulsion.

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Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.

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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.

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JAX^® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. In purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.