- decreased hematocrit / MGI
- abnormal erythropoiesis / MGI
- enlarged spleen / MGI
- anemia / MGI
- anisocytosis / MGI
- decreased hemoglobin content / MGI
- decreased erythrocyte cell number / MGI
- increased erythroid progenitor cell number / MGI
- increased sensitivity to xenobiotic induced morbidity/mortality / MGI
- increased red blood cell distribution width / MGI
STOCK Mir144/Mir451atm1.2Doca/Cnrm
Status | Available to order |
EMMA ID | EM:05328 |
International strain name | STOCK Mir144/Mir451atm1.2Doca/Cnrm |
Alternative name | Mir144/Mir451 |
Strain type | Targeted Mutant Strains : Knock-out |
Allele/Transgene symbol | Mir144/Mir451atm1.2Doca |
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. Cre-mediated recombination simultaneous deleted the hairpin that encodes miR-144 as well as the TSS for the miR-144/451 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 CRE-expressing transgenic mice (Del-Cre) to simultaneous remove the frt flanked neor cassette, the transcription start site, and miR-144. The resulting mutant mice were backcrossed to C57BL/6N to remove the CRE transgene. The offspring carrying the mutation were backcrossed 3 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 (allele matching)
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
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