Overview

Heterozygotes with JAXTag™

Also Known As:B6 nude, C57BL/6 nude

Foxn1^nu (nude) mice are born with functional but faulty hair growth follicles, resulting in a hairless appearance. These mice are also athymic, and consequently homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. They can be used in experiments otherwise requiring thymectomy in mice.

Genetic overview

Genetic Background	Generation
000664 C57BL/6J	Contact Technical Support (2018-08-27 00:00:00)

Foxn1^nu

Allele Type	Gene Symbol	Gene Name
Spontaneous (Null/Knockout)	Foxn1	forkhead box N1

View Genetics

Research Applications

Research Tools
Internal/Organ Research
Dermatology Research
Endocrine Deficiency Research
Immunology, Inflammation and Autoimmunity Research

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Base Price

Starting at:

$232.19 Domestic price for female 4-week

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Details

Detailed Description

The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1^nu, formerly Hfh11^nu) are abnormal hair growth and defective development of the thymic epithelium. Although the mice appear hairless, they are born with functional but faulty hair growth follicles. Hair growth cycles and patterns are evident especially in pigmented mice but the faulty follicles do not allow the hair to properly erupt. Homozygous pups can be identified as young as 24 hours by their lack of whiskers or poorly developed, crinkled whiskers. Nude mice are also athymic caused by a developmental failure of the thymic anlage. Consequently, homozygous nude mice lack T cells and suffer from a lack of cell-mediated immunity. However there is not a defect in T-cell precursors, and under the right conditions some functional mature T cells can be found especially in adult mice. Because of a defect in helper T-cell activity, responses to thymus-dependent antigens when detectable are primarily limited to IgM. Homozygous nude mice show partial defect in B cell development probably due to absence of functional T cells. Other endocrine and neurological deficiencies have been reported. The use of nude mice has reduced the number of thymectomy procedures required in research projects. Females are not effective breeders.Ovulation starts late at 2.5 months and ends early at four months.

For heterozygous mice only, this strain ships with a JAXTag^TM affixed. Learn more about JAXTag^TM.

View Flow Cytometry Characterization Data for Immunodeficient JAX Strains.

Development

The Foxn1^nu mutation was first recorded by Dr. N.R. Grist at the Virus Laboratory, Ruchill Hospital, Glasgow, Scotland. The mutation arose in a mouse stock that was closed but not inbred. The first seven backcrosses onto BALB were made using BALB/cN and the strain was imported to The Jackson Laboratory from NIH in 1975. It was bred brother (nu/nu) by sister (nu/+) for three generations before adopting the pattern of crossing a nu/nu male to a C57BL/6J female every other generation. The stock was cryopreserved in 1984 by mating nu/nu males at N14F1 to C57BL/6J females.

Control Suggestions

Heterozygote from the colony
Untyped from the colony
000664 C57BL/6J

Additional Information

Considerations for Choosing Controls

Selected References

Cordier AC; Haumont SM. 1980. Development of thymus, parathyroids, and ultimo-branchial bodies in NMRI and nude mice. Am J Anat 157(3):227-63PubMed: 7405870 MGI: J:6363
Dubey JP; Liddell S; Mattson D; Speert CA; Howe DK; Jenkins MC. 2001. Characterization of the Oregon isolate of Neospora hughesi from a horse. J Parasitol 87(2):345-53PubMed: 11318565 MGI: J:109880
Flanagan SP. 1966. 'Nude', a new hairless gene with pleiotropic effects in the mouse. Genet Res 8(3):295-309PubMed: 5980117 MGI: J:5043
Gonzalez M; Merino R; Gonzalez AL; Merino J. 1995. The ability of B cells to participate in allogeneic cognate T-B cell interactions in vitro depends on the presence of CD4+ T cells during their development. J Immunol 155(3):1091-100PubMed: 7636182 MGI: J:109914
Hirasawa T; Yamashita H; Makino S. 1998. Genetic typing of the mouse and rat nude mutations by PCR and restriction enzyme analysis. Exp Anim 47(1):63-7PubMed: 9498115 MGI: J:46550
Jenkinson EJ; Van Ewijk W; Owen JJ. 1981. Major histocompatibility complex antigen expression on the epithelium of the developing thymus in normal and nude mice. J Exp Med 153(2):280-92PubMed: 6940949 MGI: J:109960
Kaestner KH; Knochel W; Martinez DE. 2000. Unified nomenclature for the winged helix/forkhead transcription factors. Genes Dev 14(2):142-6PubMed: 10702024 MGI: J:59917
Kaushik A; Kelsoe G; Jaton JC. 1995. The nude mutation results in impaired primary antibody repertoire. Eur J Immunol 25(2):631-634PubMed: 7875225 MGI: J:23271
Nehls M; Pfeifer D; Schorpp M; Hedrich H; Boehm T. 1994. New member of the winged-helix protein family disrupted in mouse and rat nude mutations. Nature 372(6501):103-7PubMed: 7969402 MGI: J:21194
Pantelouris EM. 1968. Absence of thymus in a mouse mutant. Nature 217(126):370-1PubMed: 5639157 MGI: J:5059
Segre JA; Nemhauser JL; Taylor BA; Nadeau JH; Lander ES. 1995. Positional cloning of the nude locus: genetic, physical, and transcription maps of the region and mutations in the mouse and rat. Genomics 28(3):549-59PubMed: 7490093 MGI: J:28409

View All References

Genetics

Foxn1^nu

Allele Symbol: Foxn1^nu

Allele Name	nude
Allele Type	Spontaneous (Null/Knockout)
Allele Synonym(s)	Foxnl^nu; hairless; nu; Whn^-
Gene Symbol and Name	Foxn1, forkhead box N1
Gene Synonym(s)
Strain of Origin	albino stock
Chromosome	11
Molecular Note	A single base pair (G) deletion in exon 3 introduces a frameshift and a premature stop codon. The encoded protein is predicted to terminate upstream of the DNA-binding domain.

Disease/Phenotype

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

T-cell immunodeficiency, congenital alopecia, and nail dystrophy

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).

DiGeorge syndrome

Research Areas By Phenotype

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

Genotype: Foxn1^nu related

Research Tools
- Cancer Research
  - xenograft/transplant host
- Immunology, Inflammation and Autoimmunity Research
  - T cell deficiency
Internal/Organ Research
- Thymus Defects
Dermatology Research
- Skin and Hair Texture Defects
Endocrine Deficiency Research
- Adrenal Cortex Defects
- Skin Defects
- Thyroid Defects
Immunology, Inflammation and Autoimmunity Research
- Immunodeficiency
  - T cell deficiency

Mammalian Phenotype Terms by Genotype

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

Genotype: Foxn1^nu/Foxn1^nu
Not Specified

behavior/neurological phenotype

impaired spatial learning
- in the extinction phase spend more time in the training quadrant and are less able to recall data from the previous day's training
- replenishing mice with T cells from wild-type mice improves performance in a Morris water maze
- longer latency during the acquisition and reversal phases in a Morris water maze

growth/size/body region phenotype

decreased body size

postnatal growth retardation

decreased body weight

hematopoietic system phenotype

abnormal spleen morphology
- the proportion of red to white pulp is greater than normal
- in some cases the Malpighian follicles are present but are fewer in number and smaller than in controls

athymia

abnormal thymus morphology
- a thymic rudiment comprised of vesicles and lacking lymphoid cells is present at P1-P2
- a much smaller and dorsoventrally flattened thymic rudiment is present at E14-E15

small spleen

decreased leukocyte cell number

abnormal splenic cell ratio
- in some cases an unusually high number of megakaryocytes is seen in the red pulp

immune system phenotype

abnormal thymus morphology
- a thymic rudiment comprised of vesicles and lacking lymphoid cells is present at P1-P2
- a much smaller and dorsoventrally flattened thymic rudiment is present at E14-E15

small spleen

abnormal spleen morphology
- the proportion of red to white pulp is greater than normal
- in some cases the Malpighian follicles are present but are fewer in number and smaller than in controls

abnormal splenic cell ratio
- in some cases an unusually high number of megakaryocytes is seen in the red pulp

athymia

abnormal lymph node T cell domain morphology
- virtual absence of small lymphocytes in the thymus dependent area and the post-capillary venules are often thin walled and empty

decreased leukocyte cell number

abnormal Peyer's patch germinal center morphology
- absent

integument phenotype

absent vibrissae
- absent at birth

hairless
- in some mice, cephalo-caudal migration of an irregular band of short sparse hair
- sparse hair growth around 5 weeks of age
- mice fail to grow a first coat of hair

short vibrissae
- older mice show repeated growth and loss of short and wavy vibrissae

thin skin
- reduction in skin thickness at 3 weeks of age, corresponding to the catagen stage of normal skin

wavy vibrissae
- older mice show repeated growth and loss of short and wavy vibrissae

cardiovascular system phenotype

abnormal venule morphology
- in the thymus dependent area of the lymph nodes the post-capillary venules are often thin walled and empty

liver/biliary system phenotype

abnormal liver morphology
- variable degrees of severity, typically increasing with age at time of death
- liver lobes were atrophied and covered with red scars

mortality/aging

postnatal lethality, incomplete penetrance
- 55% mortality within 2 weeks
- some mice die within 1 week of birth

premature death
- most die within a few weeks of weaning
- 100% mortality by 25 weeks

reproductive system phenotype

reduced male fertility

coiled sperm flagellum
- many sperm had coiled tails

asthenozoospermia

small ovary

abnormal estrous cycle
- many females exhibited continuous dioestrus and metaoestrus phases

female infertility
- severely reduced fertility

cellular phenotype

coiled sperm flagellum
- many sperm had coiled tails

asthenozoospermia

endocrine/exocrine gland phenotype

abnormal thymus morphology
- a thymic rudiment comprised of vesicles and lacking lymphoid cells is present at P1-P2
- a much smaller and dorsoventrally flattened thymic rudiment is present at E14-E15

athymia

small ovary

Genotype: Foxn1^nu/Foxn1^nu
involves: NMRI

embryo phenotype

abnormal embryonic tissue morphology
- at the end of the 11th day the pharyngo-branchial duct is reduced to a thin cord of cells that later disappears and the cervical duct also degenerates
- the cervical duct has not narrowed and the third cleft covers only the dorsal part of the third branchial pouch at E1.5
- the ectoderm of the third cleft covers only the distal extremity and a small part of the cranial and caudal walls of the third pouch at E11.5

immune system phenotype

abnormal thymus development
- at E12.5 the primitive thymus is essentially endodermal with the ectodermal portion confined to the cranial region
- at E12 the ectoderm covers only the mid-portion of the ventral and external surfaces of the endoderm
- at no time is the epithelium invaded by lymphoid cells
- between E12 and E14 the volume of the thymus merely doubles rather than growing exponentially as in controls and the epithelial mass does not increase from E14 to E16

integument phenotype

abnormal hair cortex keratinization
- impaired

abnormal hair cortex morphology
- missing irregularly in the zone of final hardening
- the cortex of the intrafollicular part of the hair shaft is always fragmented into globular and irregularly formed aggregates and includes unusual filamentous substances

abnormal hair cuticle
- missing irregularly in the zone of final hardening
- either discontinuous or more frequently totally absent
- occupied by abnormal globular aggregates

abnormal hair follicle morphology
- hair follicles in the zone of final hardening show pronounced pathological changes
- Normal - however, the number of hair bulbs is similar to controls

abnormal cutaneous collagen fibril morphology
- fibrils are more tightly packed than in controls

abnormal hair shaft morphology
- hair shafts below the epidermis are composed of globular and discontinuous conglomerates of horny material
- hair shafts from the flank show multiple fractures, are twisted, crippled and bent, and locally thickened by numerous fusiform bulges
- most shafts fail to reach the epidermal surface and those that do are weak and fragile

abnormal nail plate morphology
- the dorsal nail plate separates from the hyponychium but bends toward the ventral side and breaks off
- the nail plate is compact and narrows toward the tip of the nail
- sulfur content of the nail plate is reduced
- the nail plate is markedly thinner at both the proximal nail fold and the tip of the nail
- nail plates consist of smaller, elongated superficial squames with slightly irregular surfaces and serrated borders
- the nail plate appears basophilic

abnormal nail matrix morphology
- keratohyalin granules of irregular size and shape are present in the cytoplasm of the suprabasal keratinocytes and insert into the aggregated tonofilaments disturbing filament aggregation
- the matrix zone is thinner and extends farther toward the distal tip of the nail
- some suprabasal cells show increased cytoplasm often associated with multiple intracytoplasmic vacuoles
- keratinocytes high in the spinous layer show striped cytoplasm
- the matrix region is severely altered
- the ventral epithelium of the proximal nail fold and the suprabasal cells of the nail matrix lack keratin 1 immunoreactivity and show abnormal expression of filaggrin

nail dystrophy

abnormal hair follicle inner root sheath morphology
- missing irregularly in the zone of final hardening

abnormal epidermis stratum corneum morphology
- the layer is loosened with increased distance from the granular layer
- highly irregular, with areas of large piles of horny substances and projected corneocytes alternated with regions of only few and extremely attenuated corneous layers
- the lamellae are irregularly shaped and detached from one another, with intercellular contact lost over large areas

deformed nails
- blunt, broken, irregularly formed ends

short nails
- severely shortened nails
- in most mice the nails terminate at the junction of the nail plate and the hyponychium

abnormal epidermis stratum granulosum morphology
- markedly reduced number and thickness of tonofilament bundles

abnormal corneocyte morphology
- the skin surface looks rough because of bizarrely formed and projected corneocytes
- the interior of the corneocytes has an inhomogeneous appearance

abnormal epidermal layer morphology
- half-desmosomes attaching basal cells to the subjacent basal lamina are irregularly spaced with only scantly tonofilaments attached to them

reduced hair shaft melanin granule number
- pigment granules are only randomly detected in the hair cortex

abnormal epidermis stratum basale morphology
- cells contain only few and small bundles of tonofilaments

abnormal nail morphology
- Normal - the nail bed epithelium does not appear to be abnormal
- there is a prominent granular layer between the upper layers of the stratum spinosum and the nail plate

abnormal coat/ hair morphology
- sulfur content of the hair fibers is reduced

endocrine/exocrine gland phenotype

abnormal thymus development
- at E12.5 the primitive thymus is essentially endodermal with the ectodermal portion confined to the cranial region
- at E12 the ectoderm covers only the mid-portion of the ventral and external surfaces of the endoderm
- between E12 and E14 the volume of the thymus merely doubles rather than growing exponentially as in controls and the epithelial mass does not increase from E14 to E16
- at no time is the epithelium invaded by lymphoid cells

mammalian phenotype

endocrine/exocrine gland phenotype
- Normal - the structure of the parathyroid is identical to controls at E16 and E17

pigmentation phenotype

reduced hair shaft melanin granule number
- pigment granules are only randomly detected in the hair cortex

hematopoietic system phenotype

abnormal thymus development
- at E12 the ectoderm covers only the mid-portion of the ventral and external surfaces of the endoderm
- at E12.5 the primitive thymus is essentially endodermal with the ectodermal portion confined to the cranial region
- at no time is the epithelium invaded by lymphoid cells
- between E12 and E14 the volume of the thymus merely doubles rather than growing exponentially as in controls and the epithelial mass does not increase from E14 to E16

Genotype: Foxn1^nu/Foxn1^nu
involves: CBA

immune system phenotype

decreased leukocyte cell number
- decrease in the number of agranulocytes (lymphocytes plus monocytes) in the peripheral blood in older mice

abnormal spleen physiology
- fewer plaque forming cells per spleen and when normalized to the number of nucleated spleen cells following immunization with sheep red blood cells

decreased lymphocyte cell number

decreased T cell number
- Normal - no difference is detected in the number of theta antigen expressing cells in the brain
- very few theta isoantigen expressing cells are detected in the lymph nodes

abnormal T cell activation
- fewer plaque forming cells per spleen and when normalized to the number of nucleated spleen cells following immunization with sheep red blood cells
- injection of phytohaemagglutinin does not result in an increase in popliteal or inguinal node weight

abnormal lymph node morphology
- very few theta isoantigen expressing cells are detected in the lymph nodes

increased length of allograft survival

hematopoietic system phenotype

abnormal T cell activation
- injection of phytohaemagglutinin does not result in an increase in popliteal or inguinal node weight
- fewer plaque forming cells per spleen and when normalized to the number of nucleated spleen cells following immunization with sheep red blood cells

decreased T cell number
- Normal - no difference is detected in the number of theta antigen expressing cells in the brain
- very few theta isoantigen expressing cells are detected in the lymph nodes

decreased leukocyte cell number
- decrease in the number of agranulocytes (lymphocytes plus monocytes) in the peripheral blood in older mice

decreased lymphocyte cell number

Genotype: Foxn1^nu/Foxn1^nu
involves: C57BL/10Sn * C57BR/cd

endocrine/exocrine gland phenotype

abnormal thymus development
- at E16 in the thymic rudiment TR3+ cells are absent and the number of TR4+ and TR5+ cells are reduced

hematopoietic system phenotype

abnormal thymus development
- at E16 in the thymic rudiment TR3+ cells are absent and the number of TR4+ and TR5+ cells are reduced

immune system phenotype

abnormal thymus development
- at E16 in the thymic rudiment TR3+ cells are absent and the number of TR4+ and TR5+ cells are reduced

Genotype: Foxn1^nu/Foxn1⁺
C3N.Cg-Foxn1

endocrine/exocrine gland phenotype

small thymus

hematopoietic system phenotype

small thymus

immune system phenotype

small thymus

Genotype: Foxn1^nu/Foxn1^nu
involves: CD-1

endocrine/exocrine gland phenotype

athymia

hematopoietic system phenotype

athymia

homeostasis/metabolism phenotype

decreased circulating follicle stimulating hormone level

decreased circulating luteinizing hormone level

abnormal circulating gonadotropin level
- impact of immobilization stress on luteinizing hormone level is reduced compared to heterozygous controls

immune system phenotype

athymia

mammalian phenotype

endocrine/exocrine gland phenotype
- Normal - impact of immobilization stress on luteinizing hormone level is reduced compared to heterozygous controls

Genotype: Foxn1^nu/Foxn1^nu
involves: NIH Swiss

mortality/aging

premature death
- after 12 months, of age the mortality rate per month is about twice that of heterozygous controls
- Normal - when maintained under SPF conditions, mortality from 6 weeks to 12 months of age is similar to controls

Genotype: Foxn1^nu/Foxn1⁺
NFS.Cg-Foxn1

endocrine/exocrine gland phenotype

small thymus
- difference in size compared to wild-type controls increases with age
- lobes are significantly smaller at P7 and P14

abnormal thymus morphology
- thymus lobes are rimmed to a varying degree with brown fat tissue and often asymmetrical in shape

hematopoietic system phenotype

abnormal thymus morphology
- thymus lobes are rimmed to a varying degree with brown fat tissue and often asymmetrical in shape

small thymus
- difference in size compared to wild-type controls increases with age
- lobes are significantly smaller at P7 and P14

immune system phenotype

abnormal thymus morphology
- thymus lobes are rimmed to a varying degree with brown fat tissue and often asymmetrical in shape

small thymus
- difference in size compared to wild-type controls increases with age
- lobes are significantly smaller at P7 and P14

Genotype: Foxn1^nu/Foxn1^nu
involves: BALB/c

cellular phenotype

chromosomal instability
- plasmacytomas generated are near-tetraploid and contain the t(12;15) translocation

integument phenotype

deformed nails
- broken with blunt ends

abnormal nail morphology
- nail phenotype is 100% penetrant

short nails

mortality/aging

increased susceptibility to Herpesvirales infection induced morbidity/mortality
- only 2 mice survived for more than 10 days after infection and 90% of mice die by 14 days post infection

increased susceptibility to viral infection induced morbidity/mortality
- only 2 mice survived for more than 10 days after infection and 90% of mice die by 14 days post infection

neoplasm

increased plasmacytoma incidence
- plasma cells isolated from BALB/c/C57BL/6 mice generate plasmacytomas in pristane-treated BALB/c nude mice within 4-8 weeks

vision/eye phenotype

blepharitis
- more severe following infection with HSV-1 strain CJ394 compared to controls

homeostasis/metabolism phenotype

decreased circulating alanine transaminase level
- following exposure to Pseudomonas aerugiosa exotoxin

decreased circulating interleukin-6 level
- following exposure to Pseudomonas aerugiosa exotoxin

abnormal circulating cytokine level
- mice are resistant to Pseudomonas aerugiosa exotoxin-induced liver damage and decreased circulating cytokine levels, including TNF, unlike similarly treated wild-type mice

decreased circulating tumor necrosis factor level
- mice are resistant to Pseudomonas aerugiosa exotoxin-induced liver damage and circulating cytokine levels, including TNF, unlike similarly treated wild-type mice

ascites
- develop within 4-8 weeks of plasma cell transplant; ascites contains many plasma cells, some of which are multinucleated and contain high levels of IgA

decreased circulating interleukin-2 level
- following exposure to Pseudomonas aerugiosa exotoxin

immune system phenotype

blepharitis
- more severe following infection with HSV-1 strain CJ394 compared to controls

increased susceptibility to Herpesvirales infection induced morbidity/mortality
- only 2 mice survived for more than 10 days after infection and 90% of mice die by 14 days post infection

decreased circulating interleukin-6 level
- following exposure to Pseudomonas aerugiosa exotoxin

increased susceptibility to Herpesvirales infection
- extraocular disease is more severe than in heterozygous mice
- following infection with HSV-1 strain CJ394 young mice (7-10 weeks of age) develop more severe ocular disease and develop severe extra ocular disease not seen in controls

increased susceptibility to viral infection induced morbidity/mortality
- only 2 mice survived for more than 10 days after infection and 90% of mice die by 14 days post infection

decreased circulating interleukin-2 level
- following exposure to Pseudomonas aerugiosa exotoxin

decreased susceptibility to bacterial infection
- mice are resistant to Pseudomonas aerugiosa exotoxin-induced liver damage and decreased circulating cytokine levels, including TNF, unlike similarly treated wild-type mice

abnormal circulating cytokine level
- mice are resistant to Pseudomonas aerugiosa exotoxin-induced liver damage and decreased circulating cytokine levels, including TNF, unlike similarly treated wild-type mice

decreased interferon-gamma secretion
- following exposure to Pseudomonas aerugiosa exotoxin

increased susceptibility to viral infection
- following infection with HSV-1 strain CJ394 young mice (7-10 weeks of age) develop more severe ocular disease and develop severe extra ocular disease not seen in controls
- extraocular disease is more severe than in heterozygous mice

decreased circulating tumor necrosis factor level
- mice are resistant to Pseudomonas aerugiosa exotoxin-induced liver damage and circulating cytokine levels, including TNF, unlike similarly treated wild-type mice

Genotype: Foxn1^nu/Foxn1⁺
involves: BALB/c

cardiovascular system phenotype

corneal vascularization
- detected 8 to 14 days after infection with HSV-1 strain CJ394in heterozygotes but not in wild-type or homozygous mice

vision/eye phenotype

blepharitis
- more severe and lasting longer following infection with HSV-1 strain CJ394 compared to controls

corneal vascularization
- detected 8 to 14 days after infection with HSV-1 strain CJ394in heterozygotes but not in wild-type or homozygous mice

increased incidence of corneal inflammation
- develop stromal keratitis 8 days after infection with HSV-1 strain CJ394 while homozygous and wild-type mice display only slight corneal cloudiness

immune system phenotype

increased susceptibility to Herpesvirales infection
- following infection with HSV-1 strain CJ394 young mice (7-10 weeks of age) develop more severe ocular disease and develop severe extra ocular disease not seen in controls
- extensive herpetiform spread is seen, in some cases the tissue damage is so severe that the skull is exposed
- extraocular disease is less severe than in homozygous mice

increased susceptibility to viral infection
- extensive herpetiform spread is seen, in some cases the tissue damage is so severe that the skull is exposed
- extraocular disease is less severe than in homozygous mice
- following infection with HSV-1 strain CJ394 young mice (7-10 weeks of age) develop more severe ocular disease and develop severe extra ocular disease not seen in controls

blepharitis
- more severe and lasting longer following infection with HSV-1 strain CJ394 compared to controls

increased incidence of corneal inflammation
- develop stromal keratitis 8 days after infection with HSV-1 strain CJ394 while homozygous and wild-type mice display only slight corneal cloudiness

Genotype: Foxn1^nu/Foxn1^nu
NU/J

integument phenotype

abnormal nail matrix morphology
- keratinocytes high in the spinous layer show striped cytoplasm
- the ventral epithelium of the proximal nail fold and the suprabasal cells of the nail matrix lack keratin 1 immunoreactivity and show abnormal expression of filaggrin
- the matrix region is severely altered
- some suprabasal cells show increased cytoplasm often associated with multiple intracytoplasmic vacuoles
- the matrix zone is thinner and extends farther toward the distal tip of the nail
- keratohyalin granules of irregular size and shape are present in the cytoplasm of the suprabasal keratinocytes and insert into the aggregated tonofilaments disturbing filament aggregation

abnormal nail morphology
- Normal - the nail bed epithelium does not appear to be abnormal
- there is a prominent granular layer between the upper layers of the stratum spinosum and the nail plate

abnormal nail plate morphology
- the nail plate appears basophilic
- the dorsal nail plate separates from the hyponychium but bends toward the ventral side and breaks off

nail dystrophy

Genotype: Foxn1^nu/Foxn1^nu
involves: C57BL/10

muscle phenotype

abnormal muscle morphology
- elevation in hydroxyproline in the tibialis anterior and soleus muscles on a per muscle and wet weight basis at 3 weeks of age but not at 24 weeks of age

decreased skeletal muscle fiber size
- in the tibialis anterior and soleus muscles at 3 weeks of age

decreased skeletal muscle mass
- in the limb muscles at 3 weeks of age

Genotype: Foxn1^nu/Foxn1^nu
B6NTac.Cg-Foxn1/Tac

immune system phenotype

decreased susceptibility to parasitic infection
- mice showed no sign of lesion development for up to 12 to 14 weeks post-infection; after 20 weeks, all lesions remain small

Genotype: Foxn1^nu/Foxn1⁺
C.Cg-Foxn1

endocrine/exocrine gland phenotype

small thymus

hematopoietic system phenotype

small thymus

immune system phenotype

small thymus

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

Genotype: Foxn1^nu/Foxn1^nu
B6.Cg-Foxn1

skeleton phenotype

abnormal trabecular bone morphology
- reduced trabecular bone structure

increased bone mineral density
- increased at 4 weeks of age but declines later

abnormal compact bone morphology
- reduced cortical bone structure

Genotype: Foxn1^nu/Foxn1⁺
B6N.Cg-Foxn1

endocrine/exocrine gland phenotype

small thymus

hematopoietic system phenotype

small thymus

immune system phenotype

small thymus

Phenotype Information

Body Weight Information - JAX^® Mice Strain B6.Cg-Foxn1^nu/J (000819)

References

Cordier AC; Haumont SM. 1980. Development of thymus, parathyroids, and ultimo-branchial bodies in NMRI and nude mice. Am J Anat 157(3):227-63PubMed: 7405870 MGI: J:6363
Dubey JP; Liddell S; Mattson D; Speert CA; Howe DK; Jenkins MC. 2001. Characterization of the Oregon isolate of Neospora hughesi from a horse. J Parasitol 87(2):345-53PubMed: 11318565 MGI: J:109880
Flanagan SP. 1966. 'Nude', a new hairless gene with pleiotropic effects in the mouse. Genet Res 8(3):295-309PubMed: 5980117 MGI: J:5043
Gonzalez M; Merino R; Gonzalez AL; Merino J. 1995. The ability of B cells to participate in allogeneic cognate T-B cell interactions in vitro depends on the presence of CD4+ T cells during their development. J Immunol 155(3):1091-100PubMed: 7636182 MGI: J:109914
Hirasawa T; Yamashita H; Makino S. 1998. Genetic typing of the mouse and rat nude mutations by PCR and restriction enzyme analysis. Exp Anim 47(1):63-7PubMed: 9498115 MGI: J:46550
Jenkinson EJ; Van Ewijk W; Owen JJ. 1981. Major histocompatibility complex antigen expression on the epithelium of the developing thymus in normal and nude mice. J Exp Med 153(2):280-92PubMed: 6940949 MGI: J:109960
Kaestner KH; Knochel W; Martinez DE. 2000. Unified nomenclature for the winged helix/forkhead transcription factors. Genes Dev 14(2):142-6PubMed: 10702024 MGI: J:59917
Kaushik A; Kelsoe G; Jaton JC. 1995. The nude mutation results in impaired primary antibody repertoire. Eur J Immunol 25(2):631-634PubMed: 7875225 MGI: J:23271
Nehls M; Pfeifer D; Schorpp M; Hedrich H; Boehm T. 1994. New member of the winged-helix protein family disrupted in mouse and rat nude mutations. Nature 372(6501):103-7PubMed: 7969402 MGI: J:21194
Pantelouris EM. 1968. Absence of thymus in a mouse mutant. Nature 217(126):370-1PubMed: 5639157 MGI: J:5059
Segre JA; Nemhauser JL; Taylor BA; Nadeau JH; Lander ES. 1995. Positional cloning of the nude locus: genetic, physical, and transcription maps of the region and mutations in the mouse and rat. Genomics 28(3):549-59PubMed: 7490093 MGI: J:28409

Additional References

Balciunaite G; Keller MP; Balciunaite E; Piali L; Zuklys S; Mathieu YD; Gill J; Boyd R; Sussman DJ; Hollander GA. 2002. Wnt glycoproteins regulate the expression of FoxN1, the gene defective in nude mice. Nat Immunol 3(11):1102-8PubMed: 12379851 MGI: J:79949
Carvalho TL; Mota-Santos T; Cumano A; Demengeot J; Vieira P. 2001. Arrested b lymphopoiesis and persistence of activated b cells in adult interleukin 7(-/)- mice. J Exp Med 194(8):1141-50PubMed: 11602642 MGI: J:72213
Cui Z; Willingham MC; Hicks AM; Alexander-Miller MA; Howard TD; Hawkins GA; Miller MS; Weir HM; Du W; DeLong CJ. 2003. Spontaneous regression of advanced cancer: identification of a unique genetically determined, age-dependent trait in mice. Proc Natl Acad Sci U S A 100(11):6682-7PubMed: 12724523 MGI: J:83618
VanCott JL; McNeal MM; Flint J; Bailey SA; Choi AH; Ward RL. 2001. Role for T cell-independent B cell activity in the resolution of primary rotavirus infection in mice. Eur J Immunol 31(11):3380-7PubMed: 11745356 MGI: J:72616

Additional - Foxn1^nu related

Technical Support

CONTACT TECHNICAL SUPPORT

Genotyping Protocols
- Restriction Enzyme Digest:Foxn1
- Pyrosequencing:Foxn1
- End Point Analysis:Foxn1
- Standard PCR:Foxn1
- Genotyping resources and troubleshooting
Dietary Information
- LabDiet® 5K52 formulation (6% fat)
Breeding Considerations

This strain is a challenging breeder.

The immunodeficiencies of homozygous Foxn1^nu make them highly susceptible to infection by pathogens and opportunistic organisms. Consequently, they should be maintained in pathogen- and opportunist-free environments. Using proper housing techniques can increase the lifespan of nude to one similar to that of normal littermates. Culling extra normal littermates may increase the survival rate of the homozygous Foxn1^nu. However, do not decrease litter size below five (or it may cause a decrease in lactation of nursing female). This strain is now maintained using ovarian transplantation. Homozygotes can be distinguished from heterozygous siblings by whisker formation.
- Additional Breeding and Husbandry Support
Mating System
- Ovarian Transplant (Homozygous nu/nu) x Heterozygous nu/
Appearance
- pigmented, without hair
  Related Genotype: a/a Foxn1^nu/Foxn1^nu
  
  black, unaffected
  Related Genotype: a/a Foxn1^nu/+ or a/a ?/+
Citation
When using the B6.Cg-Foxn1^nu/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #000819 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

MP13 (Maximum)

Pricing & Availability

Available Now

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Heterozygous or Wild-type for Foxn1<nu>

Related Products and Services

Frozen Mouse Embryo	B6.Cg-Foxn1<nu>/J	$2595.00
Frozen Mouse Embryo	B6.Cg-Foxn1<nu>/J	$2595.00
Frozen Mouse Embryo	B6.Cg-Foxn1<nu>/J	$3373.50
Frozen Mouse Embryo	B6.Cg-Foxn1<nu>/J	$3373.50

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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. 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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Licensing Information

Phone: 207-288-6470

Email: TechTran@jax.org

Also Known As:B6 nude, C57BL/6 nude

Genetic overview

Research Applications

Base Price

Detailed Description

Development

Control Suggestions

Additional Information

Selected References

Foxn1nu

Allele Symbol: Foxn1nu

Disease Terms

Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).

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: Foxn1nu related

Mammalian Phenotype Terms by Genotype

Genotype: Foxn1nu/Foxn1nuNot Specified

behavior/neurological phenotype

growth/size/body region phenotype

hematopoietic system phenotype

immune system phenotype

integument phenotype

cardiovascular system phenotype

liver/biliary system phenotype

mortality/aging

reproductive system phenotype

cellular phenotype

endocrine/exocrine gland phenotype

Genotype: Foxn1nu/Foxn1nuinvolves: NMRI

embryo phenotype

immune system phenotype

integument phenotype

endocrine/exocrine gland phenotype

mammalian phenotype

pigmentation phenotype

hematopoietic system phenotype

Genotype: Foxn1nu/Foxn1nuinvolves: CBA

immune system phenotype

hematopoietic system phenotype

Genotype: Foxn1nu/Foxn1nuinvolves: C57BL/10Sn * C57BR/cd

endocrine/exocrine gland phenotype

hematopoietic system phenotype

immune system phenotype

Genotype: Foxn1nu/Foxn1+C3N.Cg-Foxn1

endocrine/exocrine gland phenotype

hematopoietic system phenotype

immune system phenotype

Genotype: Foxn1nu/Foxn1nuinvolves: CD-1

endocrine/exocrine gland phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

immune system phenotype

mammalian phenotype

Genotype: Foxn1nu/Foxn1nuinvolves: NIH Swiss

mortality/aging

Genotype: Foxn1nu/Foxn1+NFS.Cg-Foxn1

endocrine/exocrine gland phenotype

hematopoietic system phenotype

immune system phenotype

Genotype: Foxn1nu/Foxn1nuinvolves: BALB/c

cellular phenotype

integument phenotype

mortality/aging

neoplasm

vision/eye phenotype

homeostasis/metabolism phenotype

immune system phenotype

Genotype: Foxn1nu/Foxn1+involves: BALB/c

cardiovascular system phenotype

vision/eye phenotype

immune system phenotype

Genotype: Foxn1nu/Foxn1nuNU/J

integument phenotype

Genotype: Foxn1nu/Foxn1nuinvolves: C57BL/10

muscle phenotype

Genotype: Foxn1nu/Foxn1nuB6NTac.Cg-Foxn1/Tac

immune system phenotype

Genotype: Foxn1nu/Foxn1+C.Cg-Foxn1

Foxn1^nu

Allele Symbol: Foxn1^nu

Genotype: Foxn1^nu related

Genotype: Foxn1^nu/Foxn1^nu
Not Specified

Genotype: Foxn1^nu/Foxn1^nu
involves: NMRI

Genotype: Foxn1^nu/Foxn1^nu
involves: CBA

Genotype: Foxn1^nu/Foxn1^nu
involves: C57BL/10Sn * C57BR/cd

Genotype: Foxn1^nu/Foxn1⁺
C3N.Cg-Foxn1

Genotype: Foxn1^nu/Foxn1^nu
involves: CD-1

Genotype: Foxn1^nu/Foxn1^nu
involves: NIH Swiss

Genotype: Foxn1^nu/Foxn1⁺
NFS.Cg-Foxn1

Genotype: Foxn1^nu/Foxn1^nu
involves: BALB/c

Genotype: Foxn1^nu/Foxn1⁺
involves: BALB/c

Genotype: Foxn1^nu/Foxn1^nu
NU/J

Genotype: Foxn1^nu/Foxn1^nu
involves: C57BL/10

Genotype: Foxn1^nu/Foxn1^nu
B6NTac.Cg-Foxn1/Tac

Genotype: Foxn1^nu/Foxn1⁺
C.Cg-Foxn1

Genotype: Foxn1^nu/Foxn1^nu
B6.Cg-Foxn1

Genotype: Foxn1^nu/Foxn1⁺
B6N.Cg-Foxn1

Additional - Foxn1^nu related