- enlarged spleen / MGI
- small thymus / MGI
- thymus hypoplasia / MGI
- abnormal T cell differentiation / MGI
- increased erythroid progenitor cell number / MGI
- decreased B cell number / MGI
- abnormal response to infection / MGI
- increased T cell proliferation / MGI
- increased T cell apoptosis / MGI
- decreased CD4-positive, alpha beta T cell number / MGI
- abnormal myeloid leukocyte morphology / MGI
- increased effector memory CD4-positive, alpha-beta T cell number / MGI
- increased effector memory CD8-positive, alpha-beta T cell number / MGI
C57BL/6J-Dckmemi/H
| Status | Available to order |
| EMMA ID | EM:06116 |
| Citation information | RRID:IMSR_EM:06116 Research Resource Identifiers (RRID) are persistent unique ID numbers assigned to help researchers cite key resources (e.g. antibodies, model organisms and software projects) in the biomedical literature to improve transparency and reproducibility in research. See https://www.rrids.org/ for more information. |
| International strain name | C57BL/6J-Dckmemi/H |
| Alternative name | dCKmemi |
| Strain type | Induced Mutant Strains : Chemically-induced |
| Allele/Transgene symbol | Dckmemi |
| Gene/Transgene symbol | Dck |
Information from provider
| Provider | Sophie Rutschmann |
| Provider affiliation | Medicine, Imperial College London |
| Genetic information | An ENU mutagenesis in a pure C57BL/6 background has induced a G to T transversion in the gene coding for deoxycytidine kinase (Dck) that results in a STOP codon for glutamic acid at position 247 (E247X). The mutant protein is functionally null. |
| Phenotypic information | A deficiency in deoxycytidine kinase affects peripheral T cell homeostatic proliferation and survival. Both B and T lymphocyte development is impaired, leading to a state of chronic lymphopenia and to a significant increase in the number of myeloid cells and erythrocytes. In the periphery, mutant lymphocytes adopt a memory phenotype, with high levels of proliferation and apoptosis, due to both cell-extrinsic and -intrinsic effects of the mutation. |
| Breeding history | Inbred, G12 |
| References |
|
| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | yes |
Information from EMMA
| Archiving centre | Mary Lyon Centre at MRC Harwell, Oxford, United Kingdom |
Disease and phenotype information
MGI phenotypes (allele matching)
MGI phenotypes (gene matching)
- extramedullary hematopoiesis / MGI
- abnormal spleen morphology / MGI
- enlarged spleen / MGI
- abnormal thymus morphology / MGI
- small thymus / MGI
- impaired hematopoiesis / MGI
- decreased IgG level / MGI
- thymus hypoplasia / MGI
- abnormal T cell differentiation / MGI
- no abnormal phenotype detected / MGI
- abnormal double-negative T cell morphology / MGI
- increased IgE level / MGI
- reticulocytosis / MGI
- increased erythroid progenitor cell number / MGI
- increased spleen weight / MGI
- decreased B cell number / MGI
- decreased T cell number / MGI
- abnormal response to infection / MGI
- absent spleen white pulp / MGI
- increased double-negative T cell number / MGI
- decreased double-positive T cell number / MGI
- increased T cell proliferation / MGI
- increased macrophage cell number / MGI
- increased T cell apoptosis / MGI
- decreased CD4-positive, alpha beta T cell number / MGI
- increased CD8-positive, alpha-beta T cell number / MGI
- increased pro-B cell number / MGI
- decreased pre-B cell number / MGI
- abnormal myeloid leukocyte morphology / MGI
- abnormal peripheral lymph node morphology / MGI
- increased effector memory CD4-positive, alpha-beta T cell number / MGI
- increased effector memory CD8-positive, alpha-beta T cell number / MGI
- decreased response to antigen / MGI
Literature references
- A deficiency in nucleoside salvage impairs murine lymphocyte development, homeostasis, and survival.;Choi Onjee, Heathcote Dean A, Ho Ka-Kei, Müller Phillip J, Ghani Hazim, Lam Eric W-F, Ashton-Rickardt Philip G, Rutschmann Sophie, ;2012;Journal of immunology (Baltimore, Md. : 1950);188;3920-7; 22407915
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