Generation of a tamoxifen inducible Tnnt2MerCreMer knock‐in mouse model for cardiac studies. Issue 6 (13th June 2015)

• Record Type: Journal Article
• Authors: Yan, Jianyun; Sultana, Nishat; Zhang, Lu; Park, David S.; Shekhar, Akshay; Hu, Jun; Bu, Lei; Cai, Chen‐Leng
• Is Part Of: Genesis. Volume 53:Issue 6(2015:Jun.)
• Page Start: 377
• Page End: 386
• Publication Date: 2015-06-13
• Subjects: Developmental genetics -- Periodicals; Genetics -- Periodicals; Developmental biology -- Periodicals; Embryology -- Periodicals; Genetic regulation -- Periodicals; 576.5
• DOI: 10.1002/dvg.22861
• Languages: English
• ISSNs: 1526-954X

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p>Tnnt2, encoding thin‐filament sarcomeric protein cardiac troponin T, plays critical roles in heart development and function in mammals. To develop an inducible genetic deletion strategy in myocardial cells, we generated a new <italic>Tnnt2:MerCreMer</italic> (<italic>Tnnt2^MerCreMer/+</italic>) knock‐in mouse. <italic>Rosa26</italic> reporter lines were used to examine the specificity and efficiency of the inducible Cre recombinase. We found that Cre was specifically and robustly expressed in the cardiomyocytes at embryonic and adult stages following tamoxifen induction. The knock‐in allele on <italic>Tnnt2</italic> locus does not impact cardiac function. These results suggest that this new <italic>Tnnt2^MerCreMer/+</italic> mouse could be applied towards the temporal genetic deletion of genes of interests in cardiomyocytes with Cre‐LoxP technology. The <italic>Tnnt2^MerCreMer/+</italic> mouse model also provides a useful tool to trace myocardial lineage during development and repair after cardiac injury. genesis 53:377–386, 2015. © 2015 Wiley Periodicals, Inc.</p> </abstract>