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Temporally controlled somatic mutagenesis in smooth muscle
S Kühbandner1, S Brummer, D Metzger
1Institut für Pharmakologie und Toxikologie, Technische Universität München, München, Germany.
Genesis (New York, N.Y. : 2000)
|October 6, 2000
Summary
We developed new mouse models for studying smooth muscle. These models use a tamoxifen-activated Cre recombinase system for efficient, long-lasting genetic engineering in smooth muscle cells.
Area of Science:
- Genetics
- Molecular Biology
- Developmental Biology
Background:
- Ligand-dependent site-specific recombinases enable precise genome engineering in mice.
- Enhancing recombination efficiency in specific somatic cell types is an ongoing research focus.
Purpose of the Study:
- To generate and characterize transgenic mouse lines for tamoxifen-inducible Cre recombinase expression in smooth muscle.
- To compare the efficiency of random transgene integration versus knock-in at the endogenous locus.
Main Methods:
- Generated transgenic mice with CreER(T2) under the SM22 promoter (random integration and knock-in).
- Administered tamoxifen to induce recombination of a reporter transgene.
- Assessed CreER(T2) expression and recombination efficiency in smooth muscle tissues.
Main Results:
- Both transgenic models expressed CreER(T2) in smooth muscle.
- Knock-in model (SM-CreER(T2)(ki)) showed higher expression and recombination efficiency than random integration (SM-CreER(T2)(tg)).
- Tamoxifen induced near-complete recombination (up to 100%) in smooth muscle cells in the knock-in model, persisting for at least four months.
Conclusions:
- The SM-CreER(T2)(ki) mouse line provides an efficient tool for studying smooth muscle biology.
- This model allows for tamoxifen-inducible, site-specific genetic manipulation in smooth muscle cells.
- These mice are valuable for investigating the impact of somatic mutations in smooth muscle research.