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Myh6-iCre Mouse Model
| Strain Name | C57BL/6NMcl-H11<sup>tm1(Myh6p romoter-NLS-iCre)</sup>/MCL |
|---|---|
| Strain Background | C57BL/6NMcl |
| Editing Type | Knock-in |
| Gene Name | Myh6/Myosin heavy chain 6 |
| Gene Synonyms | α-MHC、MyHC-α、Myhca、Myhc-a |
| NCBI No. | Gene ID: 17888 / MGI: 97255 |
| Catalog No. | M02087 |
1. Knockout or activation of cardiomyocyte potential genes
2. Research on heart formation and brand cell function
3. Research on myocardial hypertrophy, ventricular remodeling and heart rate
4. Research on archaeological diseases and archaeological restoration
5. Validation of cardiovascular disease drug targets
By precisely inserting an expression cassette comprising the Myh6 promoter, a nuclear localisation signal (NLS) sequence and an improved Cre recombinase (iCre) into the murine H11 (Hipp11) genomic safe‑harbour locus, the H11‑Myh6‑NLS‑iCre knock‑in allele was successfully generated. The H11 locus supports site‑specific integration of exogenous expression cassettes; the Myh6 promoter drives downstream iCre expression in cardiomyocytes; and the NLS sequence facilitates nuclear import of the iCre recombinase, enabling recognition of loxP sites flanking floxed alleles and mediation of DNA recombination. iCre is an improved Cre recombinase with mammalian codon optimisation, which enhances its expression level and loxP recombination efficiency in murine cells[1,2].
The Myh6 gene encodes α‑myosin heavy chain (α‑MHC), a key component of the thick filaments of the cardiac sarcomere that plays a critical role in cardiomyocyte contraction and maintenance of cardiac pumping function. The Myh6 promoter drives cardiomyocyte‑specific gene expression; therefore, H11‑Myh6‑NLS‑iCre mice can be used to achieve Cre‑mediated conditional genetic recombination in cardiomyocytes. When crossed with mice carrying floxed alleles, iCre mediates recombination between loxP sites in Myh6‑positive cardiomyocytes, enabling conditional knockout, knock‑in or reporter‑gene activation of target genes. This provides a genetic tool for studying cardiac development, cardiomyocyte maturation, cardiac hypertrophy, cardiomyopathy, cardiac injury and repair, and cardiac pharmacology[3].
References
- Browning J, Rooney M, Hams E, Takahashi S, Mizuno S, Sugiyama F, et al. Highly efficient CRISPR‑targeting of the murine Hipp11 intergenic region supports inducible human transgene expression. Mol Biol Rep. 2020;47(2):1491‑1498. doi: 10.1007/s11033‑019‑05204‑9.
- Shimshek DR, Kim J, Hübner MR, Spergel DJ, Buchholz F, Casanova E, et al. Codon‑improved Cre recombinase (iCre) expression in the mouse. Genesis. 2002;32(1):19‑26. doi: 10.1002/gene.10023.
- Huang X, Yan L, Kou S, Meng J, Lu Z, Lin CP, et al. Generation and characterization of a Myh6‑driven Cre knockin mouse line. Transgenic Res. 2021;30(6):821‑835. doi: 10.1007/s11248‑021‑00285‑4.
- Cardiomyocyte‑Specific Targeting Driven by the Myh6 (α‑MHC) promoter, iCre expression mediates Cre‑LoxP recombination predominantly in cardiomyocytes, making this model suitable for cardiac tissue and cardiomyocyte‑related research.
- Site‑Specific Integration at the H11 Locus The Myh6‑NLS‑iCre expression cassette is precisely inserted into the H11 safe‑harbour locus, minimising position effects, copy‑number variation and genetic instability associated with random integration. This supports stable and reproducible iCre expression.
- Efficient Nuclear Localisation and Recombination The NLS nuclear localisation signal facilitates iCre import into the nucleus. The codon‑optimised iCre efficiently recognises LoxP sites and mediates recombination, enhancing the efficiency of conditional gene editing in cardiomyocytes.
- Constitutive, Sustained Recombination This model does not require tamoxifen induction. Once the Myh6 promoter is activated, iCre is continuously expressed, enabling stable and persistent gene knockout, activation or reporter‑gene labelling in cardiomyocytes.
- Preservation of Endogenous Myh6 Function The expression cassette is inserted at the H11 locus without direct modification of the endogenous Myh6 gene. This leverages the cardiomyocyte‑targeting properties of the Myh6 promoter while minimising disruption to the endogenous Myh6 gene structure and α‑MHC function.
FAQ
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