Overview

Also Known As:nude

These mice carry a spontaneous, knock-out mutation at the Ces1c locus characterized by abnormal hair growth and defective development of the thymic epithelium with a lack of T cells and cell-mediated immunity.

Genetic overview

Genetic Background	Generation

Foxn1^nu

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

Marker(s)

	Marker Symbol	Marker Name
	Ces1c	carboxylesterase 1C

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Research Applications

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

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Base Price

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$2,854.50 Domestic price Cryo Recovery

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Details

Detailed Description

Mice homozygous for Ces1c^e are viable and fertile and exhibit no apparent defect.

Ces1c^e was discovered in a screen of progeny of triethylenemelamine (TEM) treated male mice for mutations at specific loci, but appears to have pre-existed in the male. The screen employed analysis of blood and kidney homogenates by "standard starch gel electrophoresis techniques" and focused on enzymes known to differ in electrophoretic mobility between the parental strains (DBA/2J and C57BL/6J). Ces1c^e was initially thought to be a null allele, but characterization of homozygous F2 mice demonstrated presence of a faint band migrating between those of the parental strains, which was not perceived in the presence of either parental band. Thus, Ces1c^e was shown to be a hypomorphic electrophoretic variant (Soares 1979).

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 deficiences 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 4 months.

Development

Ces1c^e was discovered in a specific-locus mutation screen of progeny of triethylenemelamine (TEM) mutagenized male DBA/2J mice, but appears to have been a pre-existing, spontaneous mutation. Although the TEM-treated parent was unavailable for genotyping, three lines of evidence suggest he was a heterozygous carrier of the mutation: 7 of 13 (54%) of his immediate offspring were heterozygous for Ces1c^e; he was mated within 2 weeks after TEM treatment, so these progeny were generated from sperm that were either sperm or late spermatids when exposed, ruling out a clustering effect due to mutagenesis at the spermatogonial stage; and the seven Ces1c^e/+ offspring occurred among litters of three dams (Soares 1979).

Mice of a strain/stock bearing Ces1c^e, called ES-IE, were imported from Dr. Soares, then at NIEH, by Dr. Eva Eicher. The original stock was maintained by sister-brother inbreeding. In 1982, Ces1c^e/Ces1c^e males of this stock were bred to C57BL/6J females to produce embryos for cryopreservation. These heterozygous embryos were assigned Stock No. 000785. In 1995, mice were recovered from the cryopreserved embryos to generate an F2 generation, from which mice homozygous for both Ces1c^e and a (nonagouti) were selected and bred to generate embryos for cryopreservation. These embryos, which are segregating for Tyrp1^b and Myo5a^d, were designated STOCK a/a Ces1c^e/Ces1c^e and retained Stock No. 000785.

STOCK Ces1c^e/Ces1c^e Foxn1^nu/+ (Stock No. 003118) was generated by mating a STOCK a/a Ces1c^e/Ces1c^e (Stock No. 00785) female to a C57BL/6J-Foxn1^nu/Foxn1^nu male, then selecting Ces1c^e homozygotes from the F2 as colony founders. Embryos were generated for cryopreservation by crossing Foxn1^nu/+ or Foxn1^nu/Foxn1^nu females to Foxn1^nu/+ or Foxn1^nu/Foxn1^nu males at generation F4+.

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.

Ces1c

Marker Symbol: Ces1c

Marker Synonym(s)
Chromosome(s)	8

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

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
Research Tools
- Cancer Research
  - xenograft/transplant host
- Immunology, Inflammation and Autoimmunity Research
  - T cell deficiency
Internal/Organ Research
- Thymus Defects

Mammalian Phenotype Terms by Genotype

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

Genotype: 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 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

integument phenotype

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

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

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

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

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

abnormal epidermis stratum corneum morphology
- 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
- the layer is loosened with increased distance from the granular layer

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

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

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

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 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 matrix morphology
- keratinocytes high in the spinous layer show striped cytoplasm
- 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
- some suprabasal cells show increased cytoplasm often associated with multiple intracytoplasmic vacuoles
- the matrix region is severely altered
- the matrix zone is thinner and extends farther toward the distal tip of the nail
- 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

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

deformed nails
- blunt, broken, irregularly formed ends

nail dystrophy

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

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

endocrine/exocrine gland 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

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
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
- longer latency during the acquisition and reversal phases in a Morris water maze
- replenishing mice with T cells from wild-type mice improves performance in a Morris water maze

growth/size/body region phenotype

decreased body size

decreased body weight

postnatal growth retardation

hematopoietic system phenotype

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

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

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

athymia

decreased leukocyte cell number

small spleen

immune system phenotype

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

abnormal Peyer's patch germinal center morphology
- absent

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

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

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

athymia

decreased leukocyte cell number

small spleen

integument phenotype

absent vibrissae
- absent at birth

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

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

mortality/aging

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

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

reproductive system phenotype

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

asthenozoospermia

coiled sperm flagellum
- many sperm had coiled tails

female infertility
- severely reduced fertility

reduced male fertility

small ovary

cellular phenotype

asthenozoospermia

coiled sperm flagellum
- many sperm had coiled tails

endocrine/exocrine gland phenotype

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

athymia

small ovary

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^nu
involves: BALB/c

cellular phenotype

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

homeostasis/metabolism phenotype

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

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 alanine transaminase level
- following exposure to Pseudomonas aerugiosa exotoxin

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

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

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

integument phenotype

abnormal nail morphology
- nail phenotype is 100% penetrant

deformed nails
- broken with blunt ends

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

immune system phenotype

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

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

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

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

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

decreased interferon-gamma secretion
- 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

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 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
- 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

Genotype: Foxn1^nu/Foxn1⁺
C.Cg-Foxn1

endocrine/exocrine gland phenotype

small thymus

hematopoietic system phenotype

small thymus

immune system phenotype

small thymus

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^nu
NU/J

integument phenotype

abnormal nail matrix morphology
- keratinocytes high in the spinous layer show striped cytoplasm
- 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
- some suprabasal cells show increased cytoplasm often associated with multiple intracytoplasmic vacuoles
- the matrix region is severely altered
- the matrix zone is thinner and extends farther toward the distal tip of the nail
- 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

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

nail dystrophy

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

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

increased susceptibility to Herpesvirales 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

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

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

endocrine/exocrine gland 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

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⁺
B6N.Cg-Foxn1

endocrine/exocrine gland phenotype

small thymus

hematopoietic system phenotype

small thymus

immune system phenotype

small thymus

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: 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
involves: CD-1

endocrine/exocrine gland phenotype

athymia

hematopoietic system phenotype

athymia

homeostasis/metabolism phenotype

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

decreased circulating follicle stimulating hormone level

decreased circulating luteinizing hormone level

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: CBA

hematopoietic system phenotype

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

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

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

immune system phenotype

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

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

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

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

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

increased length of allograft survival

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

References

Additional 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
Flanagan SP. 1966. 'Nude', a new hairless gene with pleiotropic effects in the mouse. Genet Res 8(3):295-309PubMed: 5980117 MGI: J:5043
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
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
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
Soares ER. 1979. Identification of a new allele of Es-I segregating in an inbred strain of mice. Biochem Genet 17(7-8):577-83PubMed: 540008 MGI: J:6287

Additional - Ces1c related

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
Citation
When using the nude mouse strain in a publication, please cite the originating article(s) and include JAX stock #003118 in your Materials and Methods section.

Animal Health Reports

Facility Barrier Level Descriptions

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

Pricing & Availability

Cryo Recovery

Domestic
International

Live Mouse

Age

Genotype

Price

weeks

Cryorecovery - Pricing

Service/Product	Description	Price
	Homozygous for Es1<e>, Heterozygous or Homozygous for Foxn1<nu>, 1 pair minimum

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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.

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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"). "PRODUCT(S)" means biological materials supplied by JACKSON, and their derivatives. "SERVICES" means projects conducted by JACKSON for other parties that may include but are not limited to the use of MICE or PRODUCTS. "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 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, PRODUCTS or SERVICES from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON’s prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED "AS IS". JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

Credit for PRODUCTS or SERVICES

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of, PRODUCTS or SERVICES, JACKSON will, at its option, provide credit or replacement for the PRODUCT received or the SERVICES provided; JACKSON makes no other representations and this shall be the exclusive remedy of the purchaser. Please note specific policy for live mice.

Animal Care and Use for SERVICES

Consistent with the requirement for a written understanding regarding animal care and use, the JACKSON Animal Care and Use Committee will review the animal care and use protocol(s) associated with any SERVICES to be performed at JACKSON, and JACKSON shall have ultimate responsibility and authority for the care of animals while on site or in JACKSON custody.

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. Unless prohibited by law, 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, PRODUCTS or SERVICES 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.

Also Known As:nude

Genetic overview

Marker(s)

Research Applications

Base Price

Detailed Description

Development

Foxn1nu

Allele Symbol: Foxn1nu

Ces1c

Marker Symbol: Ces1c

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/Foxn1nuinvolves: NMRI

embryo phenotype

immune system phenotype

integument phenotype

endocrine/exocrine gland phenotype

mammalian phenotype

pigmentation phenotype

hematopoietic system phenotype

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/Foxn1nuB6NTac.Cg-Foxn1/Tac

immune system phenotype

Genotype: Foxn1nu/Foxn1nuinvolves: BALB/c

cellular phenotype

homeostasis/metabolism phenotype

integument phenotype

mortality/aging

neoplasm

vision/eye phenotype

immune system phenotype

Genotype: Foxn1nu/Foxn1+C.Cg-Foxn1

endocrine/exocrine gland phenotype

hematopoietic system phenotype

immune system phenotype

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

endocrine/exocrine gland phenotype

hematopoietic system phenotype

immune system phenotype

Genotype: Foxn1nu/Foxn1nuNU/J

integument phenotype

Genotype: Foxn1nu/Foxn1+involves: BALB/c

cardiovascular system phenotype

vision/eye phenotype

immune system phenotype

Genotype: Foxn1nu/Foxn1+NFS.Cg-Foxn1

endocrine/exocrine gland phenotype

hematopoietic system phenotype

immune system phenotype

Genotype: Foxn1nu/Foxn1+B6N.Cg-Foxn1

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: C57BL/10

muscle phenotype

Genotype: Foxn1nu/Foxn1nuinvolves: CD-1

endocrine/exocrine gland phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

Foxn1^nu

Allele Symbol: Foxn1^nu

Genotype: Foxn1^nu related

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

Genotype: Foxn1^nu/Foxn1^nu
Not Specified

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

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

Genotype: Foxn1^nu/Foxn1⁺
C.Cg-Foxn1

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

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

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

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

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

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

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

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

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

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

Additional - Foxn1^nu related