| First Author | Yan J | Year | 2015 |
| Journal | PLoS One | Volume | 10 |
| Issue | 7 | Pages | e0133472 |
| PubMed ID | 26204265 | Mgi Jnum | J:233991 |
| Mgi Id | MGI:5788632 | Doi | 10.1371/journal.pone.0133472 |
| Citation | Yan J, et al. (2015) A Murine Myh6MerCreMer Knock-In Allele Specifically Mediates Temporal Genetic Deletion in Cardiomyocytes after Tamoxifen Induction. PLoS One 10(7):e0133472 |
| abstractText | A mouse model that mediates temporal, specific, and efficient myocardial deletion with Cre-LoxP technology will be a valuable tool to determine the function of genes during heart formation. Mhy6 encodes a cardiac muscle specific protein: alpha-myosin heavy chain. Here, we generated a new Myh6-MerCreMer (Myh6(MerCreMer/+)) inducible Cre knock-in mouse by inserting a MerCreMer cassette into the Myh6 start codon. By crossing knock-in mice with Rosa26 reporter lines, we found the Myh6(MerCreMer/+) mice mediate complete Cre-LoxP recombination in cardiomyocytes after tamoxifen induction. X-gal staining and immunohistochemistry analysis revealed that Myh6-driven Cre recombinase was specifically activated in cardiomyocytes at embryonic and adult stages. Furthermore, echocardiography showed that Myh6(MerCreMer/+) mice maintained normal cardiac structure and function before and after tamoxifen administration. These results suggest that the new Myh6(MerCreMer/+) mouse can serve as a robust tool to dissect the roles of genes in heart development and function. Additionally, myocardial progeny during heart development and after cardiac injury can be traced using this mouse line. |
