IMPC phenotypes (gene matching)
B6.129-Prdm1tm4.1Liz/RobH
| Status | Available to order |
| EMMA ID | EM:08498 |
| Citation information | RRID:IMSR_EM:08498 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 | B6.129-Prdm1tm4.1Liz/RobH |
| Alternative name | Prdm1 tm4Rob |
| Strain type | Targeted Mutant Strains : Knock-in |
| Allele/Transgene symbol | Prdm1tm4.1Liz |
| Gene/Transgene symbol | Prdm1 |
Information from provider
| Provider | Elizabeth Robertson |
| Provider affiliation | The Sir William Dunn School of Pathology, University of Oxford |
| Genetic information | The Prdm1 ex6+7 fusion allele eliminates the intronic region and thus permits expression of full-length Prdm1 only |
| Phenotypic information | Homozygous:Prdm1 ex6+7/ex6+7 mice are born at Mendelian ratios, are healthy and fertile as adults, and display no visible abnormalities or signs of diseaseHeterozygous:No observed phenotype in Prdm1 +/ex6+7 mice |
| Breeding history | Generations backcrossed is >10 |
| References |
|
| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | yes |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | Mary Lyon Centre at MRC Harwell, Oxford, United Kingdom |
Disease and phenotype information
MGI phenotypes (gene matching)
- double outlet right ventricle / MGI
- oligodactyly / MGI
- abnormal myotome development / MGI
- abnormal embryo development / MGI
- decreased embryo size / MGI
- abnormal placenta morphology / MGI
- abnormal placenta development / MGI
- decreased trophoblast giant cell number / MGI
- abnormal placenta labyrinth morphology / MGI
- hemorrhage / MGI
- no abnormal phenotype detected / MGI
- abnormal germ cell morphology / MGI
- abnormal aortic valve morphology / MGI
- abnormal pharyngeal arch morphology / MGI
- abnormal primordial germ cell migration / MGI
- no phenotypic analysis / MGI
- embryonic growth retardation / MGI
- right aortic arch / MGI
- abnormal dermomyotome development / MGI
- abnormal spongiotrophoblast layer morphology / MGI
- abnormal dorsal aorta morphology / MGI
- absent oocytes / MGI
- decreased testis weight / MGI
- uterine hemorrhage / MGI
- azoospermia / MGI
- immune system phenotype / MGI
- hematopoietic system phenotype / MGI
- abnormal third pharyngeal arch morphology / MGI
- absent second pharyngeal arch / MGI
- absent plasma cells / MGI
- decreased primordial germ cell number / MGI
- absent primordial germ cells / MGI
- abnormal splenocyte physiology / MGI
- atrioventricular septal defect / MGI
- vascular ring / MGI
- abnormal left subclavian artery morphology / MGI
- absent third pharyngeal arch / MGI
- postnatal lethality, incomplete penetrance / MGI
- prenatal lethality, complete penetrance / MGI
- embryonic lethality during organogenesis, complete penetrance / MGI
- lethality throughout fetal growth and development, incomplete penetrance / MGI
- abnormal pharyngeal arch mesenchyme morphology / MGI
Literature references
- Alternative splicing regulates Prdm1/Blimp-1 DNA binding activities and corepressor interactions.;Morgan Marc A J, Mould Arne W, Li Li, Robertson Elizabeth J, Bikoff Elizabeth K, ;2012;Molecular and cellular biology;32;3403-13; 22733990