Strain Name: |
B6C3Fe a/a-Dh/J |
|---|---|
Stock Number: |
000209 |
Availability: | Repository-Cryopreserved |
General Terms and Conditions |
| Former Name |
B6C3Fe-a/a-Dh (Changed: 15-DEC-04
) |
| Genes & Alleles | Dh; a; |
Type JAX® GEMM® Strain - Mutant Stock Additional information on JAX® GEMM® Strains. Species laboratory mouse Generation N74p Appearance
black
Related Genotype: a/aStrain Description
A spontaneous mutation on chromosome 1 of the dominant hemimelia gene, Dh, causes a defect in the embryonic splanchnic mesoderm and induces congenital absence of the spleen and widespread visceral and skeletal abnormalities. Mice homozygous for the Dh mutation die shortly after birth. Heterozygotes may exhibit tibial hemimelia, polydactyly, and extra fused toes. Rear leg(s) may be held at an odd angle with bent rear ankles. Heterozygotes have enlarged lymph nodes and elevated numbers of circulating lymphocytes, granulocytes and thrombocytes. They show reduced serum IgM and IgG2 and impaired humoral antibody response as well as decreased numbers of lymph node mast cells. The Pde6brd1 allele contributed to this strain by C3FeLe.B6-a causes blindness and is segregating in this strain.
| Allele Symbol | Dh | ||
|---|---|---|---|
| Allele Name | dominant hemimelia | ||
| Strain of Origin | crossbred stock carrying a translocation | ||
| General Note | This mutation arose spontaneously in a crossbred stock carrying a translocation at the Institute of Animal Genetics, Edinburgh (J:13384). Heterozygotes show preaxial polydactyly or oligodactyly of the hindlimbs, tibial hemimelia, and sometimes reduction of the femur and pubic element of the pelvic girdle. Number of ribs, sternebrae, and presacral vertebrae tends to be reduced. The spleen is entirely lacking; the stomach is somewhat smaller and the alimentary tract shorter than normal. Homozygotes usually die within a few days after birth. Abnormalities are similar to those of heterozygotes but much more severe and include also abnormalities of the urogenital system (J:112). The defects of both heterozygotes and homozygotes are traceable to early 9 1/2 day embryos in which the normal columnar or cuboidal architecture of the epithelium of the splanchnic mesoderm is defective or lacking, leading to defective morphogenesis of the gut and associated structures (J:5034). Studies on the effect of the spleenless condition on the immune system have been reviewed by Welles and Battisto (J:30753). These studies have shown that in Dh/+ mice: the lymph nodes are enlarged; there are elevated levels of lymphocytes, granulocytes, and thrombocytes in most individuals (J:5729); there are decreased serum levels of IgM and IgG 2but normal IgG1 (J:5116); and there is normal cellular immunity (J:5492). Dh/+ mice have defective B-and T-cell co-operation in the production of IgM, probably due to defective T helpercell function (J:30753). Fletcher et al. (J:5834) concluded that absence of the spleen in Dh/+ mice significantly reduces the rate of T-cell maturation. The naturally occurring autoimmunity of strain NZB mice is significantly retarded in congenic NZB- Dh/+ mice (J:12036). Dh has been combined with Foxn1 nu (nude) to produce Dh/+ Foxn1nu/Foxn1nu mice lacking both spleen and thymus for use in immunological research (J:6062). Dh was hypothesized to be a mutation in the engrailed 1 (En1) homeobox gene but the two loci have now been shown to recombine (J:2793). | ||
| Allele Symbol | a | ||
| Allele Name | nonagouti | ||
| Allele | Control | |
|---|---|---|
| Dh | Wild-type from the colony | |
| Considerations for Choosing Controls | ||
Strains carrying a allele
View Strains carrying a (100 strains)
Strains carrying other alleles of a
View Strains carrying other alleles of a (67 strains)
Dh related
Developmental Biology Research
Internal/Organ Defects (spleen: GI)
Skeletal Defects
Immunology and Inflammation Research
Immunodeficiency Associated with Other Defects
Internal/Organ Research
Gastrointestinal Defects
Spleen Defects (asplenic)
| Strain Name: | B6C3Fe a/a-Dh/J |
| Stock Number: | 000209 |
IMPORTANT NOTE: Prices are based on shipping destination. To view prices, select your shipping destination.
| Standard Supply | Repository-Cryopreserved. Must Be Recovered. Please refer to the Supply Notes for further information. |
|---|---|
| Supply Notes |
Cryorecovery - Standard. The recovery process begins when a signed agreement form is returned to the Customer Service Department after order placement. Although results vary by strain, at least two males and two females (two pairs) will be provided, typically within 15 weeks of our receipt of the signed agreement form. If the first recovery attempt is unsuccessful or only one pair is recovered, a second recovery will be done, extending the delivery time to approximately 25 weeks. At least one member of each pair will be of known genotype and will carry the mutation if it is a mutant strain. Please note that pairs may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation of the strain. Mating schemes are sometimes modified for successful cryopreservation. Price represents a repository maintenance fee, which includes the cost of recovery of the strain from the cryopreservation resource and the periodic replacement of the frozen embryos used for recovery. Cryorecovery to establish a Dedicated Supply for greater quantities of mice. |
| Licensing | See General Terms and Conditions below |
| Control Information | View Control Information in Strain Details. |
Purchasing Information
JAX® Mice Orders
Surgical Services
Contact Information
Orders & Technical Support
Tel: 800.422.6423 or 207.288.5845
Fax: 207.288.6150
Technical Support Email Form