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- Description
- Phenotype
- Genes & alleles
- Genotyping
- Health & husbandry
- References
- Purchasing information
- Terms of Use
Description
Strain Information
Type Mutant Stock; Transgenic; Additional information on Genetically Engineered Mutant Mice. Mating System +/+ sibling x Hemizygote (Female x Male) Species laboratory mouse Generation N?+F2 (24-APR-07) Donating Investigator Judith Melki, Genopole, Inserm U798 Description
Mice hemizygous for this HSA-Cre79 transgene are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. These HSA-Cre79 transgenic mice have the cre recombinase gene driven by the human alpha-skeletal actin (HSA or ACTA1) promoter. Cre activity is restricted to adult striated muscle fibers and embryonic striated muscle cells of the somites and heart. When bred with mice containing a loxP-flanked sequence of interest, Cre-mediated recombination will result in striated muscle-specific deletion of the flanked genome. Specifically, these HSA-Cre79 (or ACTA1-Cre) transgenic mice were originally used to breed with mice heterozygous for a deletion of exon 7 and a loxP-flanked exon 7 mutation on homologous chromosomes of the Smn1 gene (see Stock No. 006138 or Stock No. 006146). The resulting offspring (heterozygous for the deletion in all cells and homozygous for the deletion in striated muscle cells) have extremely reduced lifespan characterized by progressive muscle necrosis and paralysis, and represent a model of spinal muscular atrophy (SMA). Additional SMA strains expressing cre in neurons are available as well (see Stock No. 005938, Stock No. 006297, and Stock No. 006663).HSA-Cre79 transgenic mice are available on different genetic backgrounds (see Stock No. 005936, Stock No. 006139, and Stock No. 006149).
Importation of this model was supported by the Spinal Muscular Atrophy Foundation. Creation and development was supported by the National Institute of Health and Medical Research of France (Inserm) and the Association Française contre les Myopathies (AFM). An additional help was provided by Families of SMA (U.S.A.) and Andrew’s Buddies (U.S.A.).
Development
A targeting vector was designed to place a cre recombinase gene (preceded by the rabbit beta-globin intron and followed by the SV40 polyadenylation signal) under control of the human alpha-skeletal actin promoter. This construct was microinjected into (C57BL6 x SJL)F1 embryos and implanted into pseudopregnant CD1 foster mothers. Founder 79 was bred to C57BL/6 to generate transgenic mice. At different points while maintaining this strain, transgenic mice were bred with C57BL/6 wildtype mice and/or mice harboring a loxP-flanked exon 7 mutation (Smn1tm1Jme or SMNF7) on a C57BL/6 and "129Sv" mixed background. Because expression of this transgene is confined to muscle tissue, Cre-mediated deletion of “floxed” exons does not occur in the germline. Transgenic offspring bearing the wildtype Smn1 locus on this mixed (but predominantly B6;129) background were sent to The Jackson Laboratory by Dr. Judith Melki in April 2006.
Control Information
| Control | ||
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| Noncarrier | ||
| Considerations for Choosing Controls | ||
Related Strains
Strains carrying Tg(ACTA1-cre)79Jme allele
006149 B6.Cg-Tg(ACTA1-cre)79Jme/J 006139 FVB.Cg-Tg(ACTA1-cre)79Jme/J View Strains carrying Tg(ACTA1-cre)79Jme (2 strains)
Additional Web Information
Cre-lox Systems
Phenotype
Phenotype Information
This mouse can be used to support research in many areas including:
cre relatedNeurobiology Research
Neurodegeneration
Neuromuscular Defects
Spinal Muscular Atrophy (SMA)
Research Tools
Cre-lox System (Cre-Recombinase Expression: Germline/Embryonic Expression)
Genetics Research (Mutagenesis and Transgenesis: Cre-lox System)
Neurobiology Research
Research Tools
Cre-lox System
Genetics Research (Mutagenesis and Transgenesis: Cre-lox System)
Genes & Alleles
Gene & Allele Information
| Allele Symbol | Tg(ACTA1-cre)79Jme | ||
|---|---|---|---|
| Allele Name | transgene insertion 79, Judith Melki | ||
| Allele Type | Transgenic (Cre/Flp) | ||
| Common Name(s) | HSA-Cre; HSA-Cre79; HSA::cre; | ||
| Mutation Made By | Judith Melki, Genopole, Inserm U798 | ||
| Strain of Origin | (C57BL/6J x SJL)F1 | ||
| Site of Expression | adult striated muscle fibers and embryonic striated muscle cells of the somites and heart | ||
| Expressed Gene | cre, cre recombinase, bacteriophage P1 | ||
| Cre recombinase is an enzyme derived from the bacteriophage P1 that specifically recognizes loxP sites. Cre has been shown to effectively mediate the excision of DNA located between loxP sites. After the excision event, the DNA ends recombine leaving a single loxP site in place of the intervening sequence. | |||
| Promoter | ACTA1, actin, alpha 1, skeletal muscle, human | ||
| Molecular Note | This transgene expresses Cre recombinase under the control of a human alpha-skeletal actin promoter, active in striated muscle, heart, and skeletal muscle. [MGI Ref ID J:67906] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Generic Cre Melt Curve Analysis, MCA, vers. 1
Generic Cre, STD PCR, vers. 1
Helpful Links
Optimizing PCR Protocols
References
References
Selected Reference(s)
Miniou P; Tiziano D; Frugier T; Roblot N; Le Meur M; Melki J. 1999. Gene targeting restricted to mouse striated muscle lineage. Nucleic Acids Res 27(19):e27. [PubMed: 10481039] [MGI Ref ID J:67906]
Additional References
Cifuentes-Diaz C; Frugier T; Tiziano FD; Lacene E; Roblot N; Joshi V; Moreau MH; Melki J. 2001. Deletion of murine smn exon 7 directed to skeletal muscle leads to severe muscular dystrophy. J Cell Biol 152(5):1107-14. [PubMed: 11238465] [MGI Ref ID J:67884]
Tg(ACTA1-cre)79Jme relatedBuj-Bello A; Laugel V; Messaddeq N; Zahreddine H; Laporte J; Pellissier JF; Mandel JL. 2002. The lipid phosphatase myotubularin is essential for skeletal muscle maintenance but not for myogenesis in mice. Proc Natl Acad Sci U S A 99(23):15060-5. [PubMed: 12391329] [MGI Ref ID J:81791]
Charvet C; Houbron C; Parlakian A; Giordani J; Lahoute C; Bertrand A; Sotiropoulos A; Renou L; Schmitt A; Melki J; Li Z; Daegelen D; Tuil D. 2006. New role for serum response factor in postnatal skeletal muscle growth and regeneration via the interleukin 4 and insulin-like growth factor 1 pathways. Mol Cell Biol 26(17):6664-74. [PubMed: 16914747] [MGI Ref ID J:112113]
Cheusova T; Khan MA; Schubert SW; Gavin AC; Buchou T; Jacob G; Sticht H; Allende J; Boldyreff B; Brenner HR; Hashemolhosseini S. 2006. Casein kinase 2-dependent serine phosphorylation of MuSK regulates acetylcholine receptor aggregation at the neuromuscular junction. Genes Dev 20(13):1800-16. [PubMed: 16818610] [MGI Ref ID J:110237]
Cifuentes-Diaz C; Frugier T; Tiziano FD; Lacene E; Roblot N; Joshi V; Moreau MH; Melki J. 2001. Deletion of murine smn exon 7 directed to skeletal muscle leads to severe muscular dystrophy. J Cell Biol 152(5):1107-14. [PubMed: 11238465] [MGI Ref ID J:67884]
Escher P; Lacazette E; Courtet M; Blindenbacher A; Landmann L; Bezakova G; Lloyd KC; Mueller U; Brenner HR. 2005. Synapses form in skeletal muscles lacking neuregulin receptors. Science 308(5730):1920-3. [PubMed: 15976301] [MGI Ref ID J:99246]
Gaudel C; Schwartz C; Giordano C; Abumrad NA; Grimaldi PA. 2008. Pharmacological activation of PPARbeta promotes rapid and calcineurin-dependent fiber remodeling and angiogenesis in mouse skeletal muscle. Am J Physiol Endocrinol Metab 295(2):E297-304. [PubMed: 18492772] [MGI Ref ID J:140074]
Gheyara AL; Vallejo-Illarramendi A; Zang K; Mei L; St-Arnaud R; Dedhar S; Reichardt LF. 2007. Deletion of integrin-linked kinase from skeletal muscles of mice resembles muscular dystrophy due to alpha 7 beta 1-integrin deficiency. Am J Pathol 171(6):1966-77. [PubMed: 18055553] [MGI Ref ID J:128949]
Jaworski A; Burden SJ. 2006. Neuromuscular synapse formation in mice lacking motor neuron- and skeletal muscle-derived Neuregulin-1. J Neurosci 26(2):655-61. [PubMed: 16407563] [MGI Ref ID J:104252]
Jaworski A; Smith CL; Burden SJ. 2007. GA-Binding Protein Is Dispensable for Neuromuscular Synapse Formation and Synapse-Specific Gene Expression. Mol Cell Biol 27(13):5040-6. [PubMed: 17485447] [MGI Ref ID J:121823]
Li XM; Dong XP; Luo SW; Zhang B; Lee DH; Ting AK; Neiswender H; Kim CH; Carpenter-Hyland E; Gao TM; Xiong WC; Mei L. 2008. Retrograde regulation of motoneuron differentiation by muscle beta-catenin. Nat Neurosci 11(3):262-8. [PubMed: 18278041] [MGI Ref ID J:135587]
Luquet S; Lopez-Soriano J; Holst D; Fredenrich A; Melki J; Rassoulzadegan M; Grimaldi PA. 2003. Peroxisome proliferator-activated receptor delta controls muscle development and oxidative capability. FASEB J 17(15):2299-301. [PubMed: 14525942] [MGI Ref ID J:127917]
Nicole S; Desforges B; Millet G; Lesbordes J; Cifuentes-Diaz C; Vertes D; Cao ML; De Backer F; Languille L; Roblot N; Joshi V; Gillis JM; Melki J. 2003. Intact satellite cells lead to remarkable protection against Smn gene defect in differentiated skeletal muscle. J Cell Biol 161(3):571-82. [PubMed: 12743106] [MGI Ref ID J:83343]
O'Leary DA; Noakes PG; Lavidis NA; Kola I; Hertzog PJ; Ristevski S. 2007. Targeting of the ETS factor GABPalpha disrupts neuromuscular junction synaptic function. Mol Cell Biol 27(9):3470-80. [PubMed: 17325042] [MGI Ref ID J:121356]
Prins KW; Lowe DA; Ervasti JM. 2008. Skeletal muscle-specific ablation of gamma(cyto)-actin does not exacerbate the mdx phenotype. PLoS ONE 3(6):e2419. [PubMed: 18545671] [MGI Ref ID J:137146]
Schuler M; Ali F; Chambon C; Duteil D; Bornert JM; Tardivel A; Desvergne B; Wahli W; Chambon P; Metzger D. 2006. PGC1alpha expression is controlled in skeletal muscles by PPARbeta, whose ablation results in fiber-type switching, obesity, and type 2 diabetes. Cell Metab 4(5):407-14. [PubMed: 17084713] [MGI Ref ID J:129759]
Sonnemann KJ; Fitzsimons DP; Patel JR; Liu Y; Schneider MF; Moss RL; Ervasti JM. 2006. Cytoplasmic gamma-actin is not required for skeletal muscle development but its absence leads to a progressive myopathy. Dev Cell 11(3):387-97. [PubMed: 16950128] [MGI Ref ID J:112808]
Health & husbandry
Health & Colony Maintenance Information
Animal Health Reports
Room Number AX11
Colony Maintenance
Breeding & Husbandry When maintaining a live colony, these mice are bred as hemizygotes. Mating System +/+ sibling x Hemizygote (Female x Male) Diet Information LabDiet® 5K52/5K67
Purchasing information
Pricing, Supply Level & Notes, Controls, General Terms & Conditions
Pricing
| Pricing for USA, Canada and Mexico shipping destinations |
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Weeks of Age Price* Gender Genotypes Provided Individual Mouse Price $236.40 Female or Male Hemizygous for Tg(ACTA1-cre)79Jme *Price(s) in US dollars ($)
Pairs /Price* Pair Genotype $288.65 Hemizygous for Tg(ACTA1-cre)79Jme x Noncarrier $288.65 Noncarrier x Hemizygous for Tg(ACTA1-cre)79Jme
Additional Supply Details
| Supply Notes |
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| Pricing for International shipping destinations |
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Weeks of Age Price* Gender Genotypes Provided Individual Mouse Price $307.40 Female or Male Hemizygous for Tg(ACTA1-cre)79Jme *Price(s) in US dollars ($)
Pairs /Price* Pair Genotype $375.30 Hemizygous for Tg(ACTA1-cre)79Jme x Noncarrier $375.30 Noncarrier x Hemizygous for Tg(ACTA1-cre)79Jme
Additional Supply Details
| Supply Notes |
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Supply Details
| Standard Supply | Repository-Live. A collection of over 1000 strains maintained as live colonies. Individual colonies are sized to meet current customer demand. Delivery for orders of 10 mice or less ranges on average from one to eight weeks; mice are generally shipped between four to six weeks of age with a maximum shipping age of ~nine weeks. Colony sizes do not generally support stringent age specifications for large volumes of mice; however custom orders and larger quantities of mice are easily arranged. Estimated ship dates for all orders provided within 48 hours of order placement. |
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Control Information
| Control | ||
|---|---|---|
| Noncarrier | ||
| Considerations for Choosing Controls | ||
| USA, Canada and Mexico - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
| International - Control Pricing Information for Genetically Engineered Mutant Strains. | ||
General Terms and Conditions
See Terms of Use
The Jackson Laboratory's Genotype Promise
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.Ordering and Purchasing Information
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Tel: 800.422.6423 or 207.288.5845
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Technical Support Email Form
Terms of Use
Terms of Use
General Terms and Conditions
Effective September 26, 2007: License Requirements for Strains using Cre-lox Technology only apply in Canada, see Licenses for Strains using Cre-lox Technology.
For additional Licensing and Use Restrictions view the link(s) below:
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Contact information
General inquiries
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| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
JAX® Mice & Services Conditions of Use
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