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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Irf4tm1Rdf
targeted mutation 1, Riccardo Dalla-Favera
MGI:3664434
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
ht1
Irf4tm1Rdf/Irf4tm1.1Rdf involves: 129S1/Sv * 129S4/SvJae * C57BL/6 MGI:3712441
cn2
Irf4tm1Rdf/Irf4tm1.1Rdf involves: 129S1/Sv * 129S4/SvJae * C57BL/6 MGI:3712442
cn3
Ighg1tm1(cre)Cgn/Ighg1+
Irf4tm1Rdf/Irf4tm1.1Rdf
involves: 129P2/OlaHsd * 129S1/Sv * 129S4/SvJaeSor * C57BL/6 MGI:3712440
cn4
Irf4tm1Rdf/Irf4tm1Rdf
Tg(Ucp1-cre)1Evdr/0
involves: 129S1/Sv * C57BL/6J * FVB MGI:6112615


Genotype
MGI:3712441
ht1
Allelic
Composition
Irf4tm1Rdf/Irf4tm1.1Rdf
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Irf4tm1.1Rdf mutation (0 available); any Irf4 mutation (28 available)
Irf4tm1Rdf mutation (1 available); any Irf4 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• following immunization with a T-dependent antigen, mice show normal percentages of splenic IgD+. CD23+, and PNA+ B cells, germinal centers, and IgG1 and IgM plasma cells, similar to heterozygous Irf4tm1.1Pth mice or doubly heterozygous Irf4tm1Pth / Irf4tm1.1Pth mice
• splenic and peripheral blood B cells show normal T-dependent B cell responses NP hapten, and V(H) rearrangements show similar frequencies of somatic hypermutation




Genotype
MGI:3712442
cn2
Allelic
Composition
Irf4tm1Rdf/Irf4tm1.1Rdf
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Irf4tm1.1Rdf mutation (0 available); any Irf4 mutation (28 available)
Irf4tm1Rdf mutation (1 available); any Irf4 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
• mature B cells treated with TAT-cre to achieve in vitro deletion of Irf4 are unable to differentiate into plasma cells after LPS treatment, suggesting that it is not a consequence of the developmental stage of the B cells in mutants vs wild-type

hematopoietic system
• mature B cells treated with TAT-cre to achieve in vitro deletion of Irf4 are unable to differentiate into plasma cells after LPS treatment, suggesting that it is not a consequence of the developmental stage of the B cells in mutants vs wild-type




Genotype
MGI:3712440
cn3
Allelic
Composition
Ighg1tm1(cre)Cgn/Ighg1+
Irf4tm1Rdf/Irf4tm1.1Rdf
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129S4/SvJaeSor * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ighg1tm1(cre)Cgn mutation (3 available); any Ighg1 mutation (28 available)
Irf4tm1.1Rdf mutation (0 available); any Irf4 mutation (28 available)
Irf4tm1Rdf mutation (1 available); any Irf4 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
immune system
N
• mice form germinal centers and have similar numbers of PNAhi, B220+ B cells in spleen
• following CD40 and Il-4 stimulation, mice have smaller fraction of class-switched cells than control mice (7.4% vs 26.3%); defect appears to be downstream of Cgamma1 germline transcription
• 14 days after immunization with sheep red blood cells, mutants are observed to lack plasma cells, as recognized by CD138 expression, in spleen, peripheral blood and bone marrow
• memory B cell generation occurs in mutants after immunization with NP-KLH, but the population is maintained only partly over time; numbers of NP-binding cells are much lower 42 days after immunization compared to controls
• mice receiving a secondary immunization with antigen lack plasmablasts in the spleen that bind NP, are CD138 +ve and have low B220 expression, indicating that memory B cells cannot differentiate into plasma B cells upon antigen restimulation; B cells also lack IgG1 secretion after restimulation
• mice have much lower titer of IgG1 specific for the hapten NP (nitrophenylacetyl) than controls after immunization with NP coupled to keyhole limpet hemocyanin, but titers of other immunoglobulin classes are similar to levels in controls

hematopoietic system
• following CD40 and Il-4 stimulation, mice have smaller fraction of class-switched cells than control mice (7.4% vs 26.3%); defect appears to be downstream of Cgamma1 germline transcription
• 14 days after immunization with sheep red blood cells, mutants are observed to lack plasma cells, as recognized by CD138 expression, in spleen, peripheral blood and bone marrow
• memory B cell generation occurs in mutants after immunization with NP-KLH, but the population is maintained only partly over time; numbers of NP-binding cells are much lower 42 days after immunization compared to controls
• mice receiving a secondary immunization with antigen lack plasmablasts in the spleen that bind NP, are CD138 +ve and have low B220 expression, indicating that memory B cells cannot differentiate into plasma B cells upon antigen restimulation; B cells also lack IgG1 secretion after restimulation
• mice have much lower titer of IgG1 specific for the hapten NP (nitrophenylacetyl) than controls after immunization with NP coupled to keyhole limpet hemocyanin, but titers of other immunoglobulin classes are similar to levels in controls




Genotype
MGI:6112615
cn4
Allelic
Composition
Irf4tm1Rdf/Irf4tm1Rdf
Tg(Ucp1-cre)1Evdr/0
Genetic
Background
involves: 129S1/Sv * C57BL/6J * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Irf4tm1Rdf mutation (1 available); any Irf4 mutation (28 available)
Tg(Ucp1-cre)1Evdr mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
adipose tissue
• reduced lipogenesis in isopropetenol-treated adipocytes
• small increased when fed standard chow
• elevated when fed a high-fat diet
• in inguinal and epididymal fat pads with increased lipid content

homeostasis/metabolism
• in cold-exposed mice
• in cold-exposed mice
• when fed a high-fat diet
• when fed a high-fat diet
• when mice are fed standard chow

growth/size/body
• small increased when fed standard chow
• elevated when fed a high-fat diet
• when fed a high-fat diet despite normal food intake

cellular
• reduced in the mitochondria of brown adipocytes despite normal mitochondrial number and cristae density





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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory