JAX
Mouse Strain Datasheet - 006149
B6.Cg-Tg(ACTA1-cre)79Jme/J
Also Known As: HSA-Cre79
These transgenic mice have the cre recombinase gene driven by the human alpha-skeletal actin (HSA or ACTA1) promoter. 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. These mice are useful in study of spinal muscular atrophy (SMA).
Donating Investigator
IMR Colony, The Jackson Laboratory
Genetic overview
| Genetic Background | Generation |
|---|---|
|
N11F6
|
Tg(ACTA1-cre)79Jme
| Allele Type |
|---|
| Transgenic (Recombinase-expressing) |
Base Price
Starting at:
| $263.00 Domestic price for female |
| $337.00 Domestic price for breeder pair |
Detailed 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 also available on a different genetic background (see Stock No. 006139). In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the HSA-Cre79 phenotype could vary from that originally described on a mixed genetic background. We will modify the strain description if necessary as published results become available.
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 (HSA, ACTA1) 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 wild-type 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 the floxed exon does not occur in the germline. Thus, offspring contained either the wild-type Smn1 locus or the floxed locus; never the Smn1 deletion. Transgenic offspring bearing the wild-type Smn1 locus on this mixed (but predominantly B6;129) background were sent to The Jackson Laboratory by Dr. Judith Melki in April 2006. After arriving, mutant mice were backcrossed to C57BL/6J (Stock No. 000664) for 5-10 generations.
Expression Data
| Expressed Gene | cre, cre recombinase, bacteriophage P1 |
|---|---|
| Site of Expression | adult striated muscle fibers and embryonic striated muscle cells of the somites and heart |
Control Suggestions
Selected References
- 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: 10481039MGI: J:67906
Tg(ACTA1-cre)79Jme
Allele Symbol: Tg(ACTA1-cre)79Jme
| Allele Name | transgene insertion 79, Judith Melki |
|---|---|
| Allele Type | Transgenic (Recombinase-expressing) |
| Allele Synonym(s) | HSA-Cre; HSA-Cre79; HSA::cre |
| Gene Symbol and Name | Tg(ACTA1-cre)79Jme, transgene insertion 79, Judith Melki |
| Gene Synonym(s) | HSA-Cre; HSA-Cre79; HSA::cre |
| Promoter | ACTA1, actin, alpha 1, skeletal muscle, human |
| Expressed Gene | cre, cre recombinase, bacteriophage P1 |
| Site of Expression | adult striated muscle fibers and embryonic striated muscle cells of the somites and heart |
| Strain of Origin | (C57BL/6J x SJL)F1 |
| Chromosome | UN |
| 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. |
| Mutations Made By | Judith Melki, Genopole, Inserm U798 |
Disease Terms
Research Areas By Genotype
This mouse can be used to support research in many areas including:
- Neurobiology Research
- Neurodegeneration
- Spinal Muscular Atrophy (SMA)
- Research Tools
- Cre-lox System
- Cre Recombinase Expression
- Cre Recombinase Expression: Germline/Embryonic Expression
- Genetics Research
- Mutagenesis and Transgenesis
- Mutagenesis and Transgenesis: Cre-lox System
- Neurobiology Research
- Cre-lox System
Genotype: cre related
- Research Tools
- Cre-lox System
- Genetics Research
- Mutagenesis and Transgenesis
- Mutagenesis and Transgenesis: Cre-lox System
References
- 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: 10481039MGI: J:67906
Additional - Tg(ACTA1-cre)79Jme related
- Agrawal PB; Joshi M; Savic T; Chen Z; Beggs AH. 2012. Normal myofibrillar development followed by progressive sarcomeric disruption with actin accumulations in a mouse Cfl2 knockout demonstrates requirement of cofilin-2 for muscle maintenance. Hum Mol Genet :. PubMed: 22343409MGI: J:182571
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- 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: 16818610MGI: J:110237
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- 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: 11238465MGI: J:67884
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- Huang Z; Rivas B; Agoulnik AI. 2012. Insulin-like 3 signaling is important for testicular descent but dispensable for spermatogenesis and germ cell survival in adult mice. Biol Reprod 87(6):143. PubMed: 23100620MGI: J:194006
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- Kitajima Y; Tashiro Y; Suzuki N; Warita H; Kato M; Tateyama M; Ando R; Izumi R; Yamazaki M; Abe M; Sakimura K; Ito H; Urushitani M; Nagatomi R; Takahashi R; Aoki M. 2014. Proteasome dysfunction induces muscle growth defects and protein aggregation. J Cell Sci 127(24):5204-17. PubMed: 25380823MGI: J:218217
- Kuwahara H; Horie T; Ishikawa S; Tsuda C; Kawakami S; Noda Y; Kaneko T; Tahara S; Tachibana T; Okabe M; Melki J; Takano R; Toda T; Morikawa D; Nojiri H; Kurosawa H; Shirasawa T; Shimizu T. 2010. Oxidative stress in skeletal muscle causes severe disturbance of exercise activity without muscle atrophy. Free Radic Biol Med 48(9):1252-62. PubMed: 20156551MGI: J:158821
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- Li LO; Grevengoed TJ; Paul DS; Ilkayeva O; Koves TR; Pascual F; Newgard CB; Muoio DM; Coleman RA. 2015. Compartmentalized acyl-CoA metabolism in skeletal muscle regulates systemic glucose homeostasis. Diabetes 64(1):23-35. PubMed: 25071025MGI: J:230251
- 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: 18278041MGI: J:135587
- Liu CC; Lin YC; Chen YH; Chen CM; Pang LY; Chen HA; Wu PR; Lin MY; Jiang ST; Tsai TF; Chen RH. 2016. Cul3-KLHL20 Ubiquitin Ligase Governs the Turnover of ULK1 and VPS34 Complexes to Control Autophagy Termination. Mol Cell 61(1):84-97. PubMed: 26687681MGI: J:232813
- 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: 14525942MGI: J:127917
- McMurray F; Church CD; Larder R; Nicholson G; Wells S; Teboul L; Tung YC; Rimmington D; Bosch F; Jimenez V; Yeo GS; O'Rahilly S; Ashcroft FM; Coll AP; Cox RD. 2013. Adult onset global loss of the fto gene alters body composition and metabolism in the mouse. PLoS Genet 9(1):e1003166. PubMed: 23300482MGI: J:194922
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