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SPC-Cre-ERT2 transgenic mouse for temporal gene deletion in alveolar epithelial cells
Yao-Song Gui1, Lianmei Wang, Xinlun Tian
1Department of Respiratory Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
Abstract:
Although several Cre-loxP-based gene knockout mouse models have been generated for the study of gene function in alveolar epithelia in the lung, their applications are still limited. In this study, we developed a SPC-Cre-ER(T2) mouse model, in which a tamoxifen-inducible Cre recombinase (Cre-ER(T2)) is under the control of the human surfactant protein C (SPC) promoter. The specificity and efficiency of Cre-ER(T2) activity was first evaluated by crossing SPC-Cre-ER(T2) mouse with ROSA26R mouse, a β-galactosidase reporter strain. We found that Cre-ER(T2) was expressed in 30.7% type II alveolar epithelial cells of SPC-Cre-ER(T2)/ROSA26R mouse lung tissues in the presence of tamoxifen. We then tested the tamoxifen-inducible recombinase activity of Cre-ER(T2) in a mouse strain bearing TSC1 conditional knockout alleles (TSC1(fx/fx)). TSC1 deletion was detected in the lungs of tamoxifen treated SPC-Cre-ER(T2)/TSC1(fx/fx) mice. Therefore this SPC-Cre-ER(T2) mouse model may be a valuable tool to investigate functions of genes in lung development, physiology and disease.
Insights
A new inducible mouse model using surfactant protein C (SPC) promoter allows targeted gene knockout in lung alveolar epithelial cells. This tool aids research into lung development, physiology, and disease.
Area of Science:
- Pulmonary Biology
- Genetics
- Mouse Models
Background:
- Cre-loxP systems are crucial for studying gene function in lung alveolar epithelia.
- Existing mouse models have limitations in specificity and efficiency.
Purpose of the Study:
- To develop and validate a novel tamoxifen-inducible Cre-loxP mouse model for targeting gene expression in alveolar epithelial cells.
- To assess the specificity and efficiency of the surfactant protein C (SPC) promoter-driven Cre-ER(T2) system.
Main Methods:
- Generated a SPC-Cre-ER(T2) mouse model.
- Crossed SPC-Cre-ER(T2) mice with ROSA26R reporter mice to evaluate Cre-ER(T2) activity.
- Administered tamoxifen to induce Cre-ER(T2) activity.
- Tested recombination efficiency in TSC1 conditional knockout mice (TSC1(fx/fx)).
Main Results:
- Cre-ER(T2) expression was confirmed in 30.7% of type II alveolar epithelial cells in SPC-Cre-ER(T2)/ROSA26R mice upon tamoxifen induction.
- Successful TSC1 gene deletion was observed in the lungs of tamoxifen-treated SPC-Cre-ER(T2)/TSC1(fx/fx) mice, confirming inducible recombination.
Conclusions:
- The developed SPC-Cre-ER(T2) mouse model demonstrates specific and efficient tamoxifen-inducible Cre recombinase activity in alveolar epithelial cells.
- This model serves as a valuable tool for investigating gene functions related to lung development, physiology, and diseases.
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