IMPC phenotypes (gene matching)
B6JOlaHsd.Cg-Cdkn2atm1Rdp/Cnbc
| Status | Available to order |
| EMMA ID | EM:04766 |
| International strain name | B6JOlaHsd.Cg-Cdkn2atm1Rdp/Cnbc |
| Alternative name | Ink4a-Arf (-/-) null KO mice (P16 KO), Tyrp1<+> |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Cdkn2atm1Rdp |
| Gene/Transgene symbol | Cdkn2a |
Information from provider
| Provider | Manuel Serrano |
| Provider affiliation | Molecular Oncology, CNIO (Spanish National Cancer Research Centre) |
| Additional owner | Lluis Montoliu, CNB-CSIC, Madrid, Spain |
| Genetic information | Knock-out of cyclin-dependent kinase inhibitor 2A (Cdkn2a or Ink4a-Arf) locus. Insertion, intragenic deletion: exons E2 and E3 were deleted and replaced by a neomycin cassette. Note that both the p16Ink4a and p19ARF alternative splice transcripts are mutated in this Knock-out allele. Initially associated with the Tyrp1b/Tyrp1b "brown" mutant allele, on the same chromosome, but eventually segregated to Tyrp1+ allele, through spontaneous recombination, and backcrossed to C57BL/6JOlaHsd, where it has been maintained since, at least, 2002. |
| Phenotypic information | The mice are phenotypically black coat coloured (nonagouti, a/a) and viable, but develop spontaneous tumors at an early age (3 months for homozygous mutants, 6 months for heterozygous mutants) and are highly sensitive to carcinogenic treatments. |
| Breeding history | After recombining out the Tyrp1b mutant allele, backcrossed again to C57BL/6JOlaHsd and maintained in this inbred strain since, at least, 2002. |
| References |
|
| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | CNB-CSIC, Centro Nacional de Biotecnologia, Madrid, Spain |
| Animals used for archiving | heterozygous C57BL/6JOlaHsd, wild-type C57BL/6JOlaHsd |
| Stage of embryos | 8-cell |
Disease and phenotype information
MGI phenotypes (allele matching)
- abnormal retinal photoreceptor morphology / MGI
- microphthalmia / MGI
- cataract / MGI
- abnormal posterior eye segment morphology / MGI
- abnormal lens development / MGI
- abnormal retinal neuronal layer morphology / MGI
- persistent hyperplastic primary vitreous / MGI
- increased brain tumor incidence / MGI
- extramedullary hematopoiesis / MGI
- abnormal spleen morphology / MGI
- increased tumor incidence / MGI
- increased B cell derived lymphoma incidence / MGI
- increased sarcoma incidence / MGI
- abnormal spleen red pulp morphology / MGI
- abnormal cell cycle / MGI
- increased hemangiosarcoma incidence / MGI
- increased spleen white pulp amount / MGI
- increased cutaneous melanoma incidence / MGI
- increased fibrosarcoma incidence / MGI
- increased fibroblast proliferation / MGI
- abnormal keratinocyte physiology / MGI
- increased squamous cell carcinoma incidence / MGI
- abnormal skin physiology / MGI
- abnormal cell physiology / MGI
- delayed cellular replicative senescence / MGI
- premature death / MGI
- increased lymphoma incidence / MGI
MGI phenotypes (gene matching)
- extramedullary hematopoiesis / MGI
- abnormal spleen morphology / MGI
- thymus hyperplasia / MGI
- hindlimb paralysis / MGI
- abnormal retinal photoreceptor morphology / MGI
- increased metastatic potential / MGI
- microphthalmia / MGI
- abnormal lens morphology / MGI
- cataract / MGI
- abnormal retina morphology / MGI
- male infertility / MGI
- blindness / MGI
- neoplasm / MGI
- increased papilloma incidence / MGI
- abnormal tumor incidence / MGI
- increased tumor incidence / MGI
- increased B cell derived lymphoma incidence / MGI
- increased T cell derived lymphoma incidence / MGI
- increased sarcoma incidence / MGI
- increased fibrohistocytoma incidence / MGI
- increased carcinoma incidence / MGI
- seizures / MGI
- premature death / MGI
- abnormal eye morphology / MGI
- abnormal spleen red pulp morphology / MGI
- abnormal sperm number / MGI
- oligozoospermia / MGI
- no phenotypic analysis / MGI
- abnormal cell cycle / MGI
- retinal detachment / MGI
- testicular atrophy / MGI
- abnormal lens capsule morphology / MGI
- abnormal keratinocyte physiology / MGI
- increased hemangiosarcoma incidence / MGI
- increased tumor growth/size / MGI
- abnormal retinal inner nuclear layer morphology / MGI
- increased osteosarcoma incidence / MGI
- increased squamous cell carcinoma incidence / MGI
- increased incidence of tumors by chemical induction / MGI
- increased incidence of tumors by ionizing radiation induction / MGI
- decreased incidence of tumors by chemical induction / MGI
- increased testis weight / MGI
- decreased testis weight / MGI
- increased thymus weight / MGI
- increased double-positive T cell number / MGI
- abnormal posterior eye segment morphology / MGI
- abnormal retinal ganglion layer morphology / MGI
- reproductive system phenotype / MGI
- vision/eye phenotype / MGI
- abnormal skin physiology / MGI
- abnormal lens development / MGI
- abnormal cell physiology / MGI
- abnormal retinal neuronal layer morphology / MGI
- binocular blindness / MGI
- abnormal spermatocyte morphology / MGI
- delayed cellular replicative senescence / MGI
- increased CD4-positive, alpha beta T cell number / MGI
- increased CD8-positive, alpha-beta T cell number / MGI
- increased spleen white pulp amount / MGI
- increased lung carcinoma incidence / MGI
- increased brain tumor incidence / MGI
- increased small lymphocytic lymphoma incidence / MGI
- increased histiocytic sarcoma incidence / MGI
- increased splenocyte proliferation / MGI
- increased gastrointestinal stromal tumor incidence / MGI
- primary vitreous hyperplasia / MGI
- increased melanoma incidence / MGI
- increased cutaneous melanoma incidence / MGI
- increased acute lymphoblastic leukemia incidence / MGI
- increased fibrosarcoma incidence / MGI
- persistent hyperplastic primary vitreous / MGI
- increased fibroblast proliferation / MGI
- increased lymphoma incidence / MGI
Literature references
- A strategy to study tyrosinase transgenes in mouse melanocytes.;Lavado Alfonso, Matheu Ander, Serrano Manuel, Montoliu Lluís, ;2005;BMC cell biology;6;18; 15826307
- Role of the INK4a locus in tumor suppression and cell mortality.;Serrano M, Lee H, Chin L, Cordon-Cardo C, Beach D, DePinho R A, ;1996;Cell;85;27-37; 8620534