A murine Myh6MerCreMer knock-in allele specifically mediates temporal genetic deletion in cardiomyocytes after tamoxifen induction

Jianyun Yan; Lu Zhang; Nishat Sultana; David S. Park; Akshay Shekhar; Lei Bu; Jun Hu; Shegufta Razzaque; Chen Leng Cai

doi:10.1371/journal.pone.0133472

A murine Myh6^MerCreMer knock-in allele specifically mediates temporal genetic deletion in cardiomyocytes after tamoxifen induction

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

Research output: Contribution to journal › Article › peer-review

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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.

Original language	English
Article number	e0133472
Journal	PLoS ONE
Volume	10
Issue number	7
DOIs	https://doi.org/10.1371/journal.pone.0133472
State	Published - 23 Jul 2015

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title = "A murine Myh6MerCreMer knock-in allele specifically mediates temporal genetic deletion in cardiomyocytes after tamoxifen induction",

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 (Myh6MerCreMer/+) 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 Myh6MerCreMer/+ 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 Myh6MerCreMer/+ mice maintained normal cardiac structure and function before and after tamoxifen administration. These results suggest that the new Myh6MerCreMer/+ 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.",

author = "Jianyun Yan and Lu Zhang and Nishat Sultana and Park, {David S.} and Akshay Shekhar and Lei Bu and Jun Hu and Shegufta Razzaque and Cai, {Chen Leng}",

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AU - Yan, Jianyun

AU - Zhang, Lu

AU - Sultana, Nishat

AU - Park, David S.

AU - Shekhar, Akshay

AU - Bu, Lei

AU - Hu, Jun

AU - Razzaque, Shegufta

AU - Cai, Chen Leng

N1 - Publisher Copyright: Copyright: © 2015 Yan et al.This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

PY - 2015/7/23

Y1 - 2015/7/23

N2 - 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 (Myh6MerCreMer/+) 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 Myh6MerCreMer/+ 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 Myh6MerCreMer/+ mice maintained normal cardiac structure and function before and after tamoxifen administration. These results suggest that the new Myh6MerCreMer/+ 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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A murine Myh6MerCreMer knock-in allele specifically mediates temporal genetic deletion in cardiomyocytes after tamoxifen induction

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A murine Myh6^MerCreMer knock-in allele specifically mediates temporal genetic deletion in cardiomyocytes after tamoxifen induction