IMPC phenotypes (gene matching)
B6.129-Prdm1tm1.1Liz/RobH
| Status | Available to order |
| EMMA ID | EM:08438 |
| Citation information | RRID:IMSR_EM:08438 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-Prdm1tm1.1Liz/RobH |
| Alternative name | Prdm1 ΔEx1A/ΔEx1A(Rob) |
| Strain type | Targeted Mutant Strains : Knock-out |
| Allele/Transgene symbol | Prdm1tm1.1Liz |
| Gene/Transgene symbol | Prdm1 |
Information from provider
| Provider | Elizabeth Robertson |
| Provider affiliation | Sir William Dunn School of Pathology, University of Oxford |
| Genetic information | A targeted deletion of a 2.18kb fragment fro Prdm1 (chromosome 10: 44,178,130 to 44,180,309) containing the transcript exon 1A, a novel alternative first exon that splices directly to exon 3. This deletion generated an exon 1A null allele. |
| Phenotypic information | Homozygous:Mice with targeted exon 1A deletion show that Prdm1 expression has been eliminated in LPS-stimulated B cells and plasma cell differentiation has been blocked. Embryonic development is not disrupted, and embryos with this deletion show modestly reduced Prdm1 expression levels.Heterozygous:No phenotype. |
| Breeding history | Exact number of generations backcrossed is unknown, but is more than 10. Exact number of generations sib-mated is unknown, but is more than 10 as, after backcrossing, they were maintained by intercrossing. Currently maintained as homozygous stock. |
| References |
|
| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | yes |
| Immunocompromised | yes |
Information from EMMA
| Archiving centre | Mary Lyon Centre at MRC Harwell, Oxford, United Kingdom |
| Animals used for archiving | heterozygous C57BL/6J males |
| Breeding at archiving centre | Maintained firstly by crossing to C57BL/6J for 10 generations, then by intercrossing. |
Disease and phenotype information
MGI phenotypes (allele matching)
- oligodactyly / MGI
- abnormal germ cell morphology / MGI
- absent oocytes / MGI
- decreased testis weight / MGI
- azoospermia / MGI
- decreased primordial germ cell number / MGI
- postnatal lethality, incomplete penetrance / MGI
- lethality throughout fetal growth and development, incomplete penetrance / MGI
- absent plasma cells / MGI
- abnormal splenocyte physiology / MGI
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
- Blimp-1/Prdm1 alternative promoter usage during mouse development and plasma cell differentiation.;Morgan Marc A J, Magnusdottir Erna, Kuo Tracy C, Tunyaplin Chai, Harper James, Arnold Sebastian J, Calame Kathryn, Robertson Elizabeth J, Bikoff Elizabeth K, ;2009;Molecular and cellular biology;29;5813-27; 19737919