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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID 		Gt(ROSA)26Sortm1.1(CAG-Mirc20)Eem
targeted mutation 1.1, Edward E Morrisey
MGI:5792834
Summary 2 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
 		Gt(ROSA)26Sortm1.1(CAG-Mirc20)Eem/Gt(ROSA)26Sor+
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cf+ 		involves: 129 * C57BL/6 * FVB/N MGI:5792842
cn2
 		Gt(ROSA)26Sortm1.1(CAG-Mirc20)Eem/Gt(ROSA)26Sor+
Nkx2-5tm1(cre)Rjs/Nkx2-5+ 		involves: 129S7/SvEvBrd * C57BL/6 MGI:5792841


Genotype
MGI:5792842
cn1
Allelic
Composition		 Gt(ROSA)26Sortm1.1(CAG-Mirc20)Eem/Gt(ROSA)26Sor+
A1cfTg(Myh6-cre/Esr1*)1Jmk/A1cf+
Genetic
Background		 involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
A1cfTg(Myh6-cre/Esr1*)1Jmk mutation (5 available); any A1cf mutation (39 available)
Gt(ROSA)26Sortm1.1(CAG-Mirc20)Eem mutation (0 available); any Gt(ROSA)26Sor mutation (944 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
cardiovascular system
abnormal myocardial fiber morphology ( J:233994 )
• 2 weeks after tamoxifen-treatment, the total number of cardiomyocytes and percentage of mononucleated cardiomyocytes compared with control mice
decreased myocardial fiber size ( J:233994 )
• 2 weeks after tamoxifen-treatment
increased myocardial fiber number ( J:233994 )
• 2 weeks after tamoxifen-treatment
increased heart weight ( J:233994 )
• increased heart weight to tibia length ratio 2 weeks after tamoxifen treatment
abnormal myocardial fiber physiology ( J:233994 )
• cardiomyocytes reenter the cell cycle 8 days after tamoxifen treatment
• increased cardiomyocytes proliferation in tamoxifen treated mice following induction of myocardial infarction
decreased cardiomyocyte apoptosis ( J:233994 )
• 8 days after tamoxifen treatment
abnormal response to cardiac infarction ( J:233994 )
• following induced myocardial infarction, tamoxifen-treated mice exhibit reduced fibrotic scarring with increased myocardial tissue compared with control mice
• however, mice exhibit ventricular dilation and reduced fractional shortening and ejection fraction 3 weeks after injury

cellular
decreased cardiomyocyte apoptosis ( J:233994 )
• 8 days after tamoxifen treatment

homeostasis/metabolism
abnormal response to cardiac infarction ( J:233994 )
• following induced myocardial infarction, tamoxifen-treated mice exhibit reduced fibrotic scarring with increased myocardial tissue compared with control mice
• however, mice exhibit ventricular dilation and reduced fractional shortening and ejection fraction 3 weeks after injury

muscle
abnormal myocardial fiber morphology ( J:233994 )
• 2 weeks after tamoxifen-treatment, the total number of cardiomyocytes and percentage of mononucleated cardiomyocytes compared with control mice
decreased myocardial fiber size ( J:233994 )
• 2 weeks after tamoxifen-treatment
increased myocardial fiber number ( J:233994 )
• 2 weeks after tamoxifen-treatment
decreased cardiomyocyte apoptosis ( J:233994 )
• 8 days after tamoxifen treatment

growth/size/body
increased heart weight ( J:233994 )
• increased heart weight to tibia length ratio 2 weeks after tamoxifen treatment




Genotype
MGI:5792841
cn2
Allelic
Composition		 Gt(ROSA)26Sortm1.1(CAG-Mirc20)Eem/Gt(ROSA)26Sor+
Nkx2-5tm1(cre)Rjs/Nkx2-5+
Genetic
Background		 involves: 129S7/SvEvBrd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1.1(CAG-Mirc20)Eem mutation (0 available); any Gt(ROSA)26Sor mutation (944 available)
Nkx2-5tm1(cre)Rjs mutation (1 available); any Nkx2-5 mutation (21 available)
♀ phenotype observed in females
♂ phenotype observed in males
N normal phenotype
mortality/aging
premature death ( J:233994 )
• mice die by P28

cardiovascular system
abnormal myocardial fiber morphology ( J:233994 )
• at P17, cardiomyocytes exhibit an increase in the percentage of mononucleated and binucleated cells with a decrease in the percentage of multinucleated cells compared with control cells
• disorganized sarcomeric structure at P20
enlarged heart ( J:233994 )
• at P20
increased heart weight ( J:233994 )
• increased heart weight to tibia length ratio at P20
decreased cardiac muscle contractility ( J:233994 )
• reduced ejection fraction and fractional shortening
abnormal myocardial fiber physiology ( J:233994 )
• increased cardiomyocytes proliferation in postnatal hearts

cellular

muscle
abnormal myocardial fiber morphology ( J:233994 )
• at P17, cardiomyocytes exhibit an increase in the percentage of mononucleated and binucleated cells with a decrease in the percentage of multinucleated cells compared with control cells
• disorganized sarcomeric structure at P20
decreased cardiac muscle contractility ( J:233994 )
• reduced ejection fraction and fractional shortening

growth/size/body
enlarged heart ( J:233994 )
• at P20
increased heart weight ( J:233994 )
• increased heart weight to tibia length ratio at P20




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Send questions and comments to User Support. 		last database update
05/07/2024
MGI 6.23 		The Jackson Laboratory