Foxn1nu (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.
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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 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.
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View Flow Cytometry Characterization Data for Immunodeficient JAX Strains
The Foxn1nu 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.
|Allele Type||Spontaneous (Null/Knockout)|
|Allele Synonym(s)||Foxn1nu; nude|
|Gene Symbol and Name||Foxn1, forkhead box N1|
|Gene Synonym(s)||Hfh11; RONU; D11Bhm185e; DNA segment, Chr 11, Boehm 185, expressed; FKHL20; Hfh11; D11Bhm185e; nu; HNF-3/forkhead homolog 11; nude; WHN; Rnu; whn; Whn|
|Strain of Origin||albino stock|
|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.|
The immunodeficiencies of homozygous Foxn1nu make them highly susceptible to disease and indigenous organisms. Consequently it is preferable to maintain them in defined-flora or pathogen-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 Foxn1nu. However, do not decrease litter size below five (or it may cause a decrease in lactation of nursing female). Homozygotes can be distinguished from heterozygous siblings by whisker formation.
When using the B6.Cg-Foxn1nu/J mouse strain in a publication, please cite the originating article(s) and include JAX stock #000819 in your Materials and Methods section.
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