Fxnnull::MCK-Cre mice harbor a frataxin global knock-out allele and a cardiac/skeletal muscle-specific Cre recombinase transgene. When heterozygous for Fxnnull and hemizygous or homozygous for MCK-Cre, these double mutant mice are "phenotypically normal" and are a parental control used to generate the progressive cardiomyopathy mouse line Fxnflox/null::MCK-Cre (Stock No. 029720) - which is useful in studying Friedreich's Ataxia.
Cathleen Lutz, The Jackson Laboratory
Genetic Background | Generation |
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?+pN1F8
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Allele Type |
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Transgenic (Recombinase-expressing) |
Allele Type | Gene Symbol | Gene Name |
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Endonuclease-mediated (Null/Knockout) | Fxn | frataxin |
Starting at:
$278.00 Domestic price for female 4-week |
356.51 Domestic price for breeder pair |
Fxnnull::MCK-Cre mice harbor a frataxin global knock-out allele Fxnnull (Fxnem2.1Lutzy) and the MCK-Cre transgene (Tg(Ckmm-cre)5Khn) that has Cre recombinase expression directed to cardiac and skeletal muscle. When heterozygous for the Fxnnull allele and hemizygous or homozygous for the MCK-Cre transgene, these double mutant mice are "phenotypically normal" and only used as a parental strain to generate the early-onset cardiomyopathy model of Friedreich's Ataxia, Fxnflox/null::MCK-Cre (Stock No. 029720).
When singly heterozygous for the frataxin global null allele, mice are viable and fertile with normal lifespan. Mice homozygous for the frataxin global null allele are embryonic lethal - regardless of presence or absence of the MCK-Cre transgene.
When singly hemizygous or homozygous for the MCK-Cre transgene, mice are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities.
These Fxnnull::MCK-Cre mice (Stock No. 029100) harbor a global null allele of mouse frataxin Fxnnull (Fxnem2.1Lutzy; from Stock No. 028040) and the MCK-Cre transgene with the Ckmm promoter driving Cre recombinase expression (Tg(Ckmm-cre)5Khn; from Stock No. 006475). Each component is described below.
The frataxin floxed exon 2 allele Fxnflox (Fxnem2Lutzy) was made by Dr. Cat Lutz at The Jackson Laboratory using CRISPR/cas9 endonuclease-mediated genome editing. Plasmids encoding a signal guide RNA designed to introduce loxP sites flanking exon 2 in the Fxn gene and the CRISPR/cas9 nuclease were introduced into the cytoplasm C57BL/6J-derived fertilized eggs with well recognized pronuclei. Correctly targeted embryos were transferred to pseudopregnant females. Correctly targeted pups were identified by sequencing and PCR. Mice from founder 466 were further bred to C57BL/6J inbred mice (Stock No. 000664) to develop the frataxin floxed exon 2 colony as Stock No. 028520.
To generate the global knock-out allele Fxnnull (Fxnem2.1Lutzy), male mice carrying the floxed exon 2 allele (from Stock No. 028520) were bred to female B6N.Cg-Tg(Sox2-cre)1Amc/J (Stock No. 014094). The resulting mice (exon 2 deleted from germline) were further bred to C57BL/6J to breed out the Cre recombinase transgene. Heterozygous intercrosses were performed to confirm the embryonic lethality of the null allele. Mice heterozygous for this frataxin global knock-out allele are available as Stock No. 028040. Fxnnull mice from Stock No. 028040 were used to generate Stock No. 029100.
The Tg(Ckmm-cre) transgene (MCK-Cre) was designed by Dr. C. Ronald Kahn (Joslin Diabetes Center) to have a Cre recombinase cDNA sequence (with a SV-40 large T antigen nuclear localization signal and polyA signal) inserted in place of the translation initiation site of the Ckm gene. C57BL/6-congenic MCK-Cre line 5 mice from Stock No. 006475 were used to generate Stock No. 029100.
Expressed Gene | cre, cre recombinase, bacteriophage P1 |
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Site of Expression | skeletal and cardiac muscle |
Site of Expression | Cardiac and skeletal muscle. |
Allele Name | transgene insertion 5, C Ronald Kahn |
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Allele Type | Transgenic (Recombinase-expressing) |
Allele Synonym(s) | Ckm-cre; Ckmm-cre; Ckmm-NLS-cre; CreMck; mckCRE; MCK-cre; MCKCre+; MCK-cre5; Tg(Ckm-cre)5Khn; Tg(Ckmm-cre)1Khn |
Gene Symbol and Name | Tg(Ckmm-cre)5Khn, transgene insertion 5, C Ronald Kahn |
Gene Synonym(s) | |
Promoter | Ckm, creatine kinase, muscle, mouse, laboratory |
Expressed Gene | cre, cre recombinase, bacteriophage P1 |
Site of Expression | skeletal and cardiac muscle |
Strain of Origin | FVB |
Chromosome | UN |
Molecular Note | A 6.5 kb genomic DNA fragment of the Ckmm gene containing the promoter and enhancer 1, untranslated exon 1, 3kb of intron 1 including the enhancer 2 region, and the first 16 bp of exon 2 drives expression of a modified cre with an SV40 large T antigen nuclear localization signal. Expression is directed to the heart and skeletal muscle. |
Mutations Made By | C. Ronald Kahn, Joslin Diabetes Center |
Allele Name | endonuclease-mediated mutation 2.1, Cathy Lutz |
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Allele Type | Endonuclease-mediated (Null/Knockout) |
Allele Synonym(s) | |
Gene Symbol and Name | Fxn, frataxin |
Gene Synonym(s) | |
Site of Expression | Cardiac and skeletal muscle. |
Strain of Origin | C57BL/6J |
Chromosome | 19 |
Molecular Note | CRISPR/Cas9 genome editing was used to introduce loxP sites flanking exon 2. Cre-mediated recombination removed exon 2. |
Fxnnull::MCK-Cre mice are heterozygous for the frataxin global knockout allele Fxnnull (Fxnem2.1Lutzy) on chromosome 19 and hemizygous or homozygous for the MCK-Cre transgene (Tg(Ckmm-cre)5Khn).
Mice homozygous for the frataxin global null allele are embryonic lethal - regardless of presence or absence of the MCK-Cre transgene. As such, we maintain our live colony by breeding mice heterozygous for Fxnem2.1Lutzy and homozygous for Tg(Ckmm-cre)5Khn to mice wildtype at the Fxn locus and homozygous for Tg(Ckmm-cre)5Khn.
The expected coat color is black.
When using the Fxnnull::MCK-Cre mouse strain in a publication, please cite the originating article(s) and include JAX stock #029100 in your Materials and Methods section.
Service/Product | Description | Price |
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Heterozygous or Wildtype forÊFxn<em#Lutzy>and Hemizygous or Non carrier forÊTg(Ckmm-cre)5Khn |
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The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project. We do not guarantee breeding performance and therefore suggest that investigators order more than one breeding pair to avoid delays in their research.
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