Search Criteria: Research Area is "Developmental Biology Research: Skin and Hair Texture Defects"
| Stock Number |
Strain Name Strain Description |
Standard Supply |
| 008129 | B6(V)-Bhrd/J | Repository- Live |
| 006879 | B6.129-Scd2tm1Myz/J | Repository- Live |
| While heterozygous mice are viable and fertile, mice homozygous for this targeted allele die within 24 hours of birth. Brain tissues from homozygous mice show no expression from the targeted gene. Homozygotes exhibit neonatal lethality with 100% penetrance on this genetic background (less penetrant on 129SvEv genetic background) likely due to severe skin permeability barrier abnormalities. Null mice also have abnormal epidermal morphology and abnormal lipid homeostasis in the skin and liver. These mutant mice may be useful in studying monounsaturated fatty acid synthesis, lipid biosynthesis and metabolism, cholesterol homeostasis, and skin disease, as well as obesity and diabetes. | ||
| 004088 | B6.Cg-Foxp3sf/J | Repository- Live |
| Scurfy mice develop an X-linked lymphoproliferative disease resulting from defective T cell tolerance. Phenotypes associated with these mice include runting, scaly, crusty skin on the eyelids, ears and tails, dermal thickening, squinted eyes, cachexia, reddening and swelling of the genital papilla, and small testicles that are retained in the abdominal cavity. This disorder, which parallels X-linked autoimmunity-allergic disregulation syndrome (XLAAD) in humans, results in Coombs' test-positive anemia, hypergammaglobulinemia, a small, thin thymus, and lymphohistiocytic proliferation in the skin and lymphoid organs, with splenomegaly, lymphadenomegaly, and hepatomegaly. Foxp3sf/Y males generally die by 16-25 days of age. Transgenic expression of Foxp3 prevents scurfy disease in Foxp3sf/Y mice. Neonatal thymectomy of scurfy males ameliorates disease and increases lifespan; athymic nude Foxp3sf/Y mice do not develop scurfy
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| 006238 | B6;129S4-Thbs2tm1Bst/J | Repository- Live |
| Mice homozygous for this targeted mutation are viable and fertile. Multiple analyses has confirmed the absence of protein in embryonic and adult tissue of homozygous mice. Homozygotes exhibit skin disorders (abnormal collagen fiber patterns, reduced tensile strength, increased fragility) and skin fibroblasts have attachment defects. Mice also exhibit an increase in total density/cortical thickness of the long bones, abnormally long bleeding times, and a significant increase in blood vessel density. Homozygous mice exhibit accelerated wound healing after biopsy and accelerated/increased tumor formation following chemically-induced skin carcinogenesis. Mutant mice may be useful in studies of collagen fibrillogenesis in skin and tendons, angiogenesis and vascular pathophysiology, wound healing, chemically-induced tumor progression, and as a potential model for Ehlers Danlos syndrome. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are fre
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| 006926 | C57BL/6J-EgfrVel/J | Repository- Live |
| Mice homozygous for this mutation have an embryonic lethal phenotype, failing to develop past embryonic days 13.5. Heterozygous mice are viable, fertile, do not display any behavioral abnormalities and are born with open eyelids and curly vibrissae. Adult heterozygotes often have small eyes and corneal opacity with excessive secretions at the eyelid edges. MEFs (mouse embryonic fibroblasts) exhibit reduced migratory ability, approximately 53% of wildtype controls. Histological analysis of homozygous E12.5 embryos reveals placental defects. This mutant mouse strain may be useful in studies of development and as a visible dominant marker for the Egfr allelic series. | ||
| 005415 | RHJ/LeJ-stpm/J | Repository- Live |
| The phenotype of this mutation can be identified by a curly coat, which is different from the smooth coat of control littermates. At 3 weeks of age, mice homozygous for this new mutation have very curly coats and slightly curved vibrissae. In several weeks time the curly coat disappears but the hair retains a rough texture, and the vibrissae then appear normal. Heterozygous mice have normal smooth coats and straight whiskers. | ||
| 004623 | STOCK Tg(Fos-lacZ)34Efu/J | Repository- Live |
| These TOPGAL transgenic mice are a reporter strain that express Beta-galactosidase in the presence of the lymphoid enhancer binding factor 1/transcription factor 3 (LEF/TCF) mediated signaling pathway and activated Beta-catenin. The transgene contains the lacZ gene under the control of a regulatory sequence consisting of three consensus LEF/TCF-binding motifs upstream of a minimal c-fos promoter. Transgenic mice display TOPGAL activity (Beta-galactosidase activity) during early embryonic development in a subset of pluripotent embryonic basal cells of the epithelium and dermis of developing hair follicles, but not during the next stage of hair follicle development; formation of hair germs. TOPGAL transgene activity reappears in hair follicles at E16.5 and TOPGAL expression is strongly upregulated in the postnatal hair shaft precursor cells in both whisker and body hair anagen follicles (active periods of hair growth). TOPGAL expression ceases during catagen (regression and
..... For more information please see the full descriiption on the strain data sheet | ||
| 003509 | B6.129-Blmhtm1Geh/J | Repository-Cryopreserved |
| Bleomycin (BLM) is a clinically used glycopeptide anticancer agent. It is deaminated in vitro by BLMH. Blmh null mice have decreased viability and fertitility. Only about 65% of the expected number survive the neonatal period. Mice lacking Blmh exhibit variably penetrant tail dermatitis that resembles rodent ringtail. This resembles skin lesions in humans with pellagra, necrolytic migratory erythema, and acrodermatitis enteropathica. Null mice also are more sensitive to acute BLM lethality and develop pulmonary fibrosis following BLM treatment. | ||
| 005951 | B6.129-Dgat2tm1Rvf/J | Repository-Cryopreserved |
| Mice that are homozygous for the targeted mutation have a perinatal lethal phenotype, most fail to survive past 6 hours after birth due to dehydration, skin barrier abnormalities, hypothermia and energy deficiencies. Reduced levels of gene product (mRNA) are detected by RT-PCR analysis of brown adipose tissue and livers of neonate homozygous mutants. Growth retardation is observed in homozygous embryos after embryonic day 12.5. Newborn homozygotes are hypoglycemic and lipopenic, exhibiting reduced plasma triglyceride, free fatty acid and glucose levels and have almost no white fat tissue. Within a few hours of birth, the skin of homozygotes becomes dry and cracked. Homozygous mutants rapidly lose weight due to dehydration caused by impaired permeability barrier function. Histological analysis of skin tissue from homozygotes reveals abnormally thin epidermis and compact orthohyperkeratosis of the stratum corneum. Homozygotes surviving between 8 and 24 hours develop tail necrosis. Hetero
..... For more information please see the full descriiption on the strain data sheet | ||
| 003824 | B6.129S4-Dgat1tm1Far/J | Repository-Cryopreserved |
| Mice homozygous for the Dgat1tm1Far targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities however, homozygous mutant females exhibit a complete absence of milk production, necessitating the use of foster mothers. Dgat1 mRNA is undetectable by Northern blot analysis, and DGAT enzyme activity in a variety of tissues is either absent or shows only residual levels. Surprisingly, in DGAT deficient mice triglyceride levels and fasting serum triglycerides levels are similar to wildtype controls. Although homozygotes do not differ in body weight compared to age- and sex-matched controls, total fat pad weight is reduced. Tissue triglyceride levels are reduced 30-40% in white adipose tissue and muscle. Liver triglyceride levels tend to be lower in chow-fed DGAT-deficient mice, but high-fat feeding leads to significantly lower liver triglycerides. Changes in tissue triglyceride levels are associated with in
..... For more information please see the full descriiption on the strain data sheet | ||
| 006429 | B6.Cg-Dwh/J | Repository-Cryopreserved |
| 004161 | B6;129-Fgf7tm1Efu/J | Repository-Cryopreserved |
| Mice homozygous for this targeted allele are viable, fertile and normal in size. No Fgf7 transcript is detected. By 2 months of age, the hair coat takes on a matted/greasy appearance that becomes more prominent with age. Homozygote kidneys are markedly smaller and posses structural anomalies. Morphometric analyses indicate a reduction (~30% of wildtype) in the total number of nephrons present. Kidney development appears to be effected as early as embryonic day 16.5. This mutant mouse strain represents a model that may be useful in studies related to kidney disease. | ||
| 002622 | B6Ei.Cg-pwk/J | Repository-Cryopreserved |
| Homozygous patchwork mice have hairs that are either totally white or totally pigmented, but no diluted coloration of the hair. On a nonagouti background this produces a salt-and-pepper appearance from white hairs juxtaposed with black hairs. This occurs throughout the coat and does not vary by anatomic region. The absence of pigment in the white hairs is due to an absence of melanocytes in the hair follicles of the white hairs; functioning melanocytes are present in the hair follicles of the black hairs. The absence of melanotyes in the follicles of the white hairs results from premature death of melanoblasts during development. TUNEL staining indicates that this melanoblast death is apoptotic and begins around embryonic day 18.5. This suggests that patchwork melanoblasts can survive and function if enough survive, but fail to survive when adequately reduced in number. Analysis of aggregation chimeras between patchwork and albino donors revealed gray hairs at the boundaries bet
..... For more information please see the full descriiption on the strain data sheet | ||
| 005736 | BKS(Cg)-calre/J | Repository-Cryopreserved |
| The curly coat of this spontaneous homozygous mutant mouse (BKS.Cg m +/+ Leprdb /J-calre/J) is recognized at 10-12 days of age when hair is fully covering the body. At 2 weeks of age the coat of homozygous mutants looks very curly, and the mutants also have curly vibrissae. After several weeks, the curly phenotype is reduced; the hair becomes fuzzy in appearance, and the vibrissae straighten out and appear normal. Some mutant mice have no whiskers at wean age. Also, in older homozygous and heterzygous mice more whiskers are lost, and homozygous mutants lose more hair as they age. Homozygous mutant mice live normal life spans and breed normally. | ||
| 002758 | C3Fe.Cg-scb/J | Repository-Cryopreserved |
| Scabby is a recessive mutation that maps to chromosome 8. Homozygotes display scar tissue on the skin and tail shortly after birth with defects in hair growth in these areas. Transverse stripes particularly over the rump may be seen in the juvenile coat, but are generally absent in the adult. Webbed feet and a short and kinky or constricted tail may also be seen. Homozygotes are viable and fertile although males breed better than females. (Searle and Beechey, 1977.) | ||
| 002839 | CByJ.LAH-Dsg4lah/J | Repository-Cryopreserved |
| Mice homozygous for the Dsg4lah mutation have thicker, stiffer skin and a fine scale within a few days of birth. The epidermal keratinocytes have a hyperproliferative phenotype. These mice fail to develop normal fur, and have alopecia and shortened vibrissae. Although all hair types are found, the hair is very sparse and is shorter and more rough than normal. Rather than the normal gradual transition of keratinocytes from proliferation to differentiation in the lower hair follicle, the lanceolate hair mice show a premature, abrupt switch. Above the melanogenic zone, a swelling forms that subsequently is pushed out by continued growth of the hair shaft to become the distal tip of the hair. Lanceolate hair mice take their name from the resulting lance-head shape of the hair. Homozygotes can breed, but heterozygous females are better mothers than homozygotes. Unlike Dsg4lah-J homozygotes, Dsg4lah homozygotes do not have growth re
..... For more information please see the full descriiption on the strain data sheet | ||
| 002838 | DBA/1LacJ-Dsg4lah-J/J | Repository-Cryopreserved |
| Mice homozygous for the Dsg4lah-J mutation completely lack vibrissae and develop only very short hair that resembles peach fuzz. This is lost by a few months of age, leaving these mice bald. They are runted from birth throughout life. These mice have hyperplasia in the interfollicular epidermis that leads to thickened skin, and their skin wrinkles as they age. Transmission electron micrographs of epidermis from Dsg4lah-J homozygotes reveals acantholysis with small, poorly formed, and dislodged desmosomes. Rather than the normal gradual transition of keratinocytes from proliferation to differentiation in the lower hair follicle, the lanceolate hair mice show a premature, abrupt switch. Above the melanogenic zone a swelling forms that subsequently is pushed out by continued growth of the hair shaft to become the distal tip of the hair. Lanceolate hair mice take their name from the resulting lance-head shape of the hair. The less severely affect
..... For more information please see the full descriiption on the strain data sheet | ||
| 001595 | DW/J-Acdacd/J | Repository-Cryopreserved |
| acd/acd homozygotes can be distinguished from their wildtype (?/+) littermates by darkened pigmentation, short, curly vibrissae, smaller overall size, and abnormal pelage. Hair growth is retarded and lacks zigzag and guard hairs producing a sparse coat. There is heavy pigmentation in the nose, ears, body, feet and tail, and foci of melanin are also found in the skin and lymph nodes. Tail kinks or polydactyly of the hind feet are sometimes found and external genitalia are underdeveloped. It is rare for homozygotes to breed. Hydronephrosis is sometimes found in post-wean aged homozygotes resulting from focal hypertrophy of ureteral epithelium which causes ureteral blockage. The adrenals are abnormal in both males and females. Although the size of the medullary cells is normal, the cortical cells and nuclei are much larger than normal with nuclear inclusions and many mitochondria in the cytoplasm. These mitochondria have tubular cristae and cholesterol ester droplets, whic
..... For more information please see the full descriiption on the strain data sheet | ||
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