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Former Names STOCK Es1e Foxn1nu/J (Changed: 03-NOV-10 ) Hfh11nu (Changed: 15-DEC-04 ) Type Mutant Stock; Spontaneous Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Species laboratory mouse Generation ?+F1p (09-NOV-05)
Generation DefinitionsDescription
Mice homozygous for Ces1ce are viable and fertile and exhibit no apparent defect.Ces1ce 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). Ces1ce 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, Ces1ce was shown to be a hypomorphic electrophoretic variant (Soares 1979).
The two main defects of mice homozygous for the nude spontaneous mutation (Foxn1nu, formerly Hfh11nu) 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
Ces1ce 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 Ces1ce; 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 Ces1ce/+ offspring occurred among litters of three dams (Soares 1979).Mice of a strain/stock bearing Ces1ce, 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, Ces1ce/Ces1ce 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 Ces1ce and a (nonagouti) were selected and bred to generate embryos for cryopreservation. These embryos, which are segregating for Tyrp1b and Myo5ad, were designated STOCK a/a Ces1ce/Ces1ce and retained Stock No. 000785.
STOCK Ces1ce/Ces1ce Foxn1nu/+ (Stock No. 003118) was generated by mating a STOCK a/a Ces1ce/Ces1ce (Stock No. 00785) female to a C57BL/6J-Foxn1nu/Foxn1nu male, then selecting Ces1ce homozygotes from the F2 as colony founders. Embryos were generated for cryopreservation by crossing Foxn1nu/+ or Foxn1nu/Foxn1nu females to Foxn1nu/+ or Foxn1nu/Foxn1nu males at generation F4+.
Strains carrying Foxn1nu allele
000819 B6.Cg-Foxn1nu/J 000711 CByJ.Cg-Foxn1nu/J 007850 J:NU 002019 NU/J View Strains carrying Foxn1nu (4 strains)
Strains carrying other alleles of Ces1c
001604 B6.Cg-Ces1cb Ces1eh Gusbh/J 001601 B6.YBR-Ces1cb Ces1eh/CvJ 000785 B6;D2-a Ces1ce/EiJ 014096 C57BL/6-Ces1ctm1.1Loc/J 002503 ROP/Le-Os Ces1ca/+ Ces1ca/J 002974 STOCK Ces1ce H2d/J View Strains carrying other alleles of Ces1c (6 strains)
Strains carrying other alleles of Foxn1
000820 AKR/J-Foxn1nu-str/J 012941 B6.129(SJL)-Foxn1tm1.1Dmsu/J 000521 B6.AK-Foxn1nu-str/J 000819 B6.Cg-Foxn1nu/J 000711 CByJ.Cg-Foxn1nu/J 007850 J:NU 002019 NU/J View Strains carrying other alleles of Foxn1 (7 strains)
View Related Disease (OMIM) Terms
Related Disease (OMIM) Terms provided by MGI
T-Cell Immunodeficiency, Congenital Alopecia, and Nail Dystrophy - 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 provided by MGI
assigned by genotype
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Foxn1nu/Foxn1nu
involves: albino stock
- mortality/aging
- premature death
- most die within a few weeks of weaning (MGI Ref ID J:30772)
- integument phenotype
- hairless
- mice fail to grow a first coat of hair (MGI Ref ID J:30772)
Foxn1nu/Foxn1nu
Background Not Specified
- mortality/aging
- partial postnatal lethality
- premature death
- 100% mortality by 25 weeks (MGI Ref ID J:5043)
- endocrine/exocrine gland phenotype
- small ovary (MGI Ref ID J:5043)
- growth/size phenotype
- decreased body size (MGI Ref ID J:5043)
- decreased body weight (MGI Ref ID J:5043)
- postnatal growth retardation (MGI Ref ID J:5043)
- liver/biliary system phenotype
- abnormal liver morphology
- reproductive system phenotype
- abnormal estrous cycle
- many females exhibited continuous dioestrus and metaoestrus phases (MGI Ref ID J:5043)
- asthenozoospermia (MGI Ref ID J:5043)
- coiled sperm flagellum
- many sperm had coiled tails (MGI Ref ID J:5043)
- female infertility
- severely reduced fertility (MGI Ref ID J:5043)
- reduced male fertility (MGI Ref ID J:5043)
- small ovary (MGI Ref ID J:5043)
- hematopoietic system phenotype
- athymia (MGI Ref ID J:5059)
- decreased leukocyte cell number (MGI Ref ID J:5059)
- immune system phenotype
- athymia (MGI Ref ID J:5059)
- decreased leukocyte cell number (MGI Ref ID J:5059)
- integument phenotype
- absent vibrissae
- absent at birth (MGI Ref ID J:5043)
- hairless
- short vibrissae
- older mice show repeated growth and loss of short and wavy vibrissae (MGI Ref ID J:5043)
- thin skin
- reduction in skin thickness at 3 weeks of age, corresponding to the catagen stage of normal skin (MGI Ref ID J:5043)
- wavy vibrissae
- older mice show repeated growth and loss of short and wavy vibrissae (MGI Ref ID J:5043)
Foxn1nu/Foxn1nu
B6.Cg/NTac-Foxn1nu
- 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 (MGI Ref ID J:64283)
Foxn1nu/Foxn1nu
involves: BALB/c
- homeostasis/metabolism phenotype
- 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 (MGI Ref ID J:40405)
- tumorigenesis
- 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 (MGI Ref ID J:40405)
- cellular phenotype
- chromosomal instability
- plasmacytomas generated are near-tetraploid and contain the t(12;15) translocation (MGI Ref ID J:40405)
Foxn1nu/Foxn1nu
BALB/c-Foxn1nu
- 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 (MGI Ref ID J:50903)
- decreased circulating interleukin-2 level
- following exposure to Pseudomonas aerugiosa exotoxin (MGI Ref ID J:50903)
- decreased circulating interleukin-6 level
- following exposure to Pseudomonas aerugiosa exotoxin (MGI Ref ID J:50903)
- 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 (MGI Ref ID J:50903)
- decreased interferon-gamma secretion
- following exposure to Pseudomonas aerugiosa exotoxin (MGI Ref ID J:50903)
- 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 (MGI Ref ID J:50903)
- 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 (MGI Ref ID J:50903)
- decreased circulating interleukin-2 level
- following exposure to Pseudomonas aerugiosa exotoxin (MGI Ref ID J:50903)
- decreased circulating interleukin-6 level
- following exposure to Pseudomonas aerugiosa exotoxin (MGI Ref ID J:50903)
- 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 (MGI Ref ID J:50903)
- decreased circulating alanine transaminase level
- following exposure to Pseudomonas aerugiosa exotoxin (MGI Ref ID J:50903)
View Research Applications
Research Applications
This mouse can be used to support research in many areas including:Foxn1nu related
Dermatology Research
Skin and Hair Texture Defects
Endocrine Deficiency Research
Adrenal Cortex Defects
Skin Defects
Thyroid Defects
Immunology and Inflammation Research
Immunodeficiency
T cell deficiency
Internal/Organ Research
Thymus Defects
Research Tools
Cancer Research
xenograft/transplant host
Immunology and Inflammation Research
T cell deficiency
| Allele Symbol | Foxn1nu | ||
|---|---|---|---|
| Allele Name | nude | ||
| Allele Type | Spontaneous | ||
| Common Name(s) | Foxnlnu; Whn-; hairless; nu; | ||
| Strain of Origin | albino stock | ||
| Gene Symbol and Name | Foxn1, forkhead box N1 | ||
| Chromosome | 11 | ||
| Gene Common Name(s) | D11Bhm185e; DNA segment, Chr 11, Boehm 185, expressed; FKHL20; HNF-3/forkhead homolog 11; Hfh11; RONU; Rnu; WHN; nu; nude; | ||
| General Note | Dr. N.R. Grist found a hairless mutation in mice in the Virus Laboratory, Ruchill Hospital, Glasgow, and passed it on to the Institute of Animal Genetics at Edinburgh for study. Homozygotes are hairless from birth and most die within a few weeks after weaning (J:30772). Body growth rate,viability, and fertility are severely reduced. Hair follicles are normal at birth, but keratinization, which normally occurs in the middle third of the follicle, is faulty and the hairs do not erupt (J:5043). Epidermal keratinization is also faulty (J:466). Application of exogenous keratinocyte growth factor (fibroblast growth factor 7; see Fgf7) normalizes the follicular defect in Hfh11nu/Hfh11nu mice (J:27782). The growth retardation and ossification defects in Hfh11nu homozygous mice was attributed to athymia (J:12665), rather than to hairlessness per se (J:20342).The thymus is almost totally absent (J:5059) due to failure of development of the thymic anlage which arises from the ectoderm of the third pharyngeal pouch. The rudiment remains small and cystic. Another derivative of the third pharyngeal pouch, the parathyroid, is unaffected by the nude mutation (J:6363). Differentiation of the stroma of the thymus into cortical and medullary parts, as recognized by monoclonal antibodies, occurs by embryonic day 13 in wild-type mice. This differentiation does not occur in Hfh11nu/Hfh11nu mice (J:7898). Transplantation studies have shown that the thymic rudiment of Hfh11nu/Hfh11nu mice fails to attract lymphoid cells, but that lymphoid cells of these mice are quite normal in their ability to populate implanted normal thymuses (J:11959). The thymic rudiment can engender some T-cell subpopulations and produce some factors with important functions (J:30766).Heterozygotes (Hfh11nu/+) have a thymus about 50 to 80% as large as that of +/+ congenic controls, the size of the difference depending on strain background. The two genotypes can be distinguished by this criterion (J:7330). Hfh11nu/+ mice also show a greater susceptibility to ocular infection with Herpes simplex virus infection than do +/+ mice (J:12543).Lack of the thymus in homozygotes leads to many defects of the immune system, including depletion of lymphocytes from thymus-dependent areas of lymph nodes and spleen, a much reduced lymphocyte population composed almost entirely of B-cells, relatively normal IgM response to thymus-independent antigens, very poor response to thymus-dependent antigens including failure to reject allogeneic and xenogeneic skin and tumor grafts, and greatly increased susceptibility to infection (J:11959).B cells and bone marrow stem cells are also depressed in nude mice, partly as a secondary effect of the T-cell defect. Peripheral progenmitors of mononuclear phagocytes and granulocytes are, however, abundant, and phagocytic systems are the major defense against infection (J:30766).Viability and fertility of nude mice can be greatly increased by protecting them from infectious organisms, as under specific pathogen-free or germ-free conditions (J:30766). Nude mice are widely used as naturally thymectomized mice in investigations of the role of the thymus in immune reactions.Because of its athymia and its failure to reject xenogeneic grafts, the nude mouse has also been used as a recipient for in vivo culture and study of such grafts. As Holub (J:30766) points out, the proportion of nude mouse papers devoted to studies of the mutation, as opposed to those in which the mouse is used as an athymic culture medium, has sharply declined over time. The nude mouse is regarded as thoroughly understood, and therefore usable as a research tool. Lacunae in the knowledge of the nude mutation still do exist, however. The present revue will largely disregard the extensive literature on nude mice used as tools, and will concentrate on the biology of nude.Various endocrine disorders have been described in nude mice (J:30766). A blunting of the hypothalamus-pituitary-adrenal axis response to stress stmuli has been described that occurs at both the pituitary and adrenal levels (J:12543).The nude mouse may prove to be an interesting neurophysiological model, with reductions in various central nervous system components (J:30766). Microglial cell counts in the supraventricular corpus callosum are less in nude than in normal mice (J:20954). However, cerebellar Purkinje cell and granule cell populations due not seem to be reduced in nude animals (J:20471).Flanagan (J:5043) showed linkage of the nude mutation with Re and Pmp22 on linkage group VII. Recent studies have refined the mapping with respect to successively closer mouse genes (J:4562)(J:1905), and to microsatellite loci (J:24223). As noted above, physical and transcriptional maps have further refined the location of the mutation, making positional cloning possible (J:28409) | ||
| 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. [MGI Ref ID J:21194] | ||
| Gene Symbol and Name | Ces1c, carboxylesterase 1C | ||
| Chromosome | 8 | ||
| Gene Common Name(s) | Ces-N; Ee-1; Es-1; Es-4; Es-N; Es1; Es2; esterase 1; esterase 4; esterase related gene-N; | ||
Genotyping Protocols
Foxn1nu, Pyrosequencing
Foxn1nu, Restriction Enzyme Digest
Helpful Links
Genotyping resources and troubleshooting
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Animal Health Reports
Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, RG10/RG30.
| Pricing for USA, Canada and Mexico shipping destinations |
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Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $1980.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
Supply Notes
- Cryorecovery - Standard.
We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. The total number of animals provided, their gender and genotype will vary. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 13 and 16 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. 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).
| Pricing for International shipping destinations |
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Cryopreserved Mice - Ready for Recovery
Animals Provided
Price (US dollars $) Cryorecovery* $2574.00 At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.
Standard Supply
Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
Supply Notes
- Cryorecovery - Standard.
We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. The total number of animals provided, their gender and genotype will vary. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 13 and 16 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. 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).
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Cryopreserved. Ready for recovery. Please refer to pricing and supply notes for further information.
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
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