A Murine Myh6MerCreMer Knock-In Allele Specifically Mediates Temporal Genetic Deletion in Cardiomyocytes after Tamoxifen Induction

小鼠 Myh6MerCreMer 敲入等位基因特异性介导他莫昔芬诱导后心肌细胞中的时间性基因缺失

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作者:Jianyun Yan, Lu Zhang, Nishat Sultana, David S Park, Akshay Shekhar, Lei Bu, Jun Hu, Shegufta Razzaque, Chen-Leng Cai

Abstract

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.

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