MGI phenotypes (allele matching)
- no phenotypic analysis / MGI
B6N.129P2(Cg)-Mir144/Mir451atm1.1Doca/Cnrm
| Status | Available to order |
| EMMA ID | EM:05327 |
| Citation information | RRID:IMSR_EM:05327 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 | B6N.129P2(Cg)-Mir144/Mir451atm1.1Doca/Cnrm |
| Alternative name | Mir144/Mir451 |
| Strain type | Targeted Mutant Strains : Conditional mutation |
| Allele/Transgene symbol | Mir144/Mir451atm1.1Doca |
| Gene/Transgene symbol | Mir144 |
Information from provider
| Provider | Dónal O |
| Provider affiliation | Mouse Biology Unit, European Molecular Biology Laboratory |
| Genetic information | An FRT flanked neo cassette with a 5' loxP site was inserted upstream of the transcription initiation site (TSS) for both Mir144 and Mir451. An additional loxP site was inserted between the two microRNAs. Flp mediated recombination removed the neo cassette leaving the TSS floxed. The miR-144/451 targeting strategy allows cre-mediated deletion of the TSS for the miR-144/451 cluster, as well as the hairpin that encodes miR-144. This deletion simultaneously deletes miR-144 and transcription initiation of the cluster, leading to the loss of both miR-144 and miR-451 expression. |
| Phenotypic information | Mice deficient for the miR-144/451 cluster display a cell autonomous impairment of late erythroblast maturation, resulting in erythroid hyperplasia, splenomegaly, and a mild anemia. |
| Breeding history | Upon germ line transmission, the mice carrying the targeted allele were crossed to FLP-expressing transgenic mice (FLPeR) to remove the frt flanked Neo-resistance cassette. The resulting mice were backcrossed to C57BL/6N to remove the FLP transgene. The offspring carrying the loxP-flanked allele were backcrossed 9 generations to C57BL/6N. |
| References |
|
| Homozygous fertile | yes |
| Homozygous viable | yes |
| Homozygous matings required | no |
| Immunocompromised | no |
Information from EMMA
| Archiving centre | CNR, Consiglio Nazionale delle Ricerche, Monterotondo, Italy |
Disease and phenotype information
MGI phenotypes (gene matching)
- decreased hematocrit / MGI
- abnormal erythropoiesis / MGI
- enlarged spleen / MGI
- spleen hyperplasia / MGI
- anemia / MGI
- decreased mean corpuscular volume / MGI
- reticulocytosis / MGI
- anisocytosis / MGI
- decreased hemoglobin content / MGI
- decreased erythrocyte cell number / MGI
- no phenotypic analysis / MGI
- increased erythroid progenitor cell number / MGI
- increased spleen weight / MGI
- polychromatophilia / MGI
- decreased mean corpuscular hemoglobin / MGI
- increased cellular sensitivity to hydrogen peroxide / MGI
- abnormal physiological response to xenobiotic / MGI
- increased sensitivity to xenobiotic induced morbidity/mortality / MGI
- increased red blood cell distribution width / MGI
- increased number of Heinz bodies / MGI
- decreased catalase activity / MGI
Literature references
- The miR-144/451 locus is required for erythroid homeostasis.;Rasmussen Kasper D, Simmini Salvatore, Abreu-Goodger Cei, Bartonicek Nenad, Di Giacomo Monica, Bilbao-Cortes Daniel, Horos Rastislav, Von Lindern Marieke, Enright Anton J, O'Carroll Dónal, ;2010;The Journal of experimental medicine;207;1351-8; 20513743
- New models to study plasma cells in mouse based on the restriction of IgJ expression to antibody secreting cells;Ayala MV, Bonaud A, Bender S, Lambert JM, Lechouane F, Carrion C, Cogne M, Pascal V, Sirac C;2020;Biorxiv unrefereed preprint - full text;;;