Phenotypes associated with this allele

• Allele Symbol: Cmtm3^em1Wlh
• Allele Name: endonuclease-mediated mutation 1, WenLing Han
• Allele ID: MGI:7511808
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Cmtm3^em1Wlh/Cmtm3^em1Wlh	involves: C57BL/6	MGI:7514535

Genotype
MGI:7514535

hm1

• Allelic Composition: Cmtm3^em1Wlh/Cmtm3^em1Wlh
• Genetic Background: involves: C57BL/6

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

cardiovascular system

abnormal myocardial fiber mitochondrial morphology ( J:338327 )

♂ • TEM analysis revealed damaged cardiac mitochondrial ultrastructure in cardiomyocytes

increased myocardial fiber size ( J:338327 )

♂ • H&E and wheat germ agglutinin (WGA) staining showed an increase in cardiomyocyte cross sectional area

myocardial fiber disarray ( J:338327 )

♂ • TEM analysis showed a disordered arrangement of myofilaments in cardiomyocytes

thick interventricular septum ( J:338327 )

♂ • male mice show increased interventricular septum thickness at 8 weeks of age

enlarged heart ( J:338327 )

♂ • male mice show enlarged hearts at 8 weeks of age

cardiac hypertrophy ( J:338327 )

♂ • at 8 weeks of age, the heart weight to body weight (HW/BW) ratio and the heart weight to tibia length (HW/TL) are both significantly increased, indicating cardiac hypertrophy

♂ • mRNA and protein levels of Nppa (natriuretic peptide type A, also known as ANP) are significantly increased in heart tissue

myocardium hypertrophy ( J:338327 )

♂

increased heart left ventricle wall thickness ( J:338327 )

♂ • male mice show increased left ventricular wall thickness at 8 weeks of age

increased heart left ventricle posterior wall thickness ( J:338327 )

♂ • left ventricular posterior wall thickness is markedly increased at end-diastole

decreased cardiac muscle contractility ( J:338327 )

♂ • at 4 weeks after angiotensin II (Ang II) infusion, mice show a significant decline in the ejection fraction (EF%) and percent fractional shortening (FS%) relative to Ang II-treated wild-type controls, suggesting the decompensated period of cardiac function after Ang II infusion

increased cardiac muscle contractility ( J:338327 )

♂ • in the basal state, hypertrophic hearts exhibit a marked increase in the ejection fraction (EF%) and percent fractional shortening (FS%), likely due to the maintenance or even increased cardiac function during the compensatory stage of cardiac hypertrophy

increased response of heart to induced stress ( J:338327 )

♂ • at 4 weeks after angiotensin II (Ang II) infusion, mice show exacerbated myocardial hypertrophy with a further increase in heart size, left ventricular wall and interventricular septum thickness, HW/TL ratio and cardiomyocyte cross sectional area, more disorderly arrangement of myofilaments and more damaged cardiac mitochondrial ultrastructure, a further increase in Nppa (ANP) mRNA and protein levels, and a significant decline in the ejection fraction (EF%) and percent fractional shortening (FS%) relative to Ang II-treated wild-type controls

homeostasis/metabolism

increased response of heart to induced stress ( J:338327 )

♂ • at 4 weeks after angiotensin II (Ang II) infusion, mice show exacerbated myocardial hypertrophy with a further increase in heart size, left ventricular wall and interventricular septum thickness, HW/TL ratio and cardiomyocyte cross sectional area, more disorderly arrangement of myofilaments and more damaged cardiac mitochondrial ultrastructure, a further increase in Nppa (ANP) mRNA and protein levels, and a significant decline in the ejection fraction (EF%) and percent fractional shortening (FS%) relative to Ang II-treated wild-type controls

abnormal hormone level ( J:338327 )

♂ • atrial natriuretic peptide (ANP) mRNA and protein levels are significantly increased in heart tissue

cellular

abnormal myocardial fiber mitochondrial morphology ( J:338327 )

♂ • TEM analysis revealed damaged cardiac mitochondrial ultrastructure in cardiomyocytes

dilated mitochondrion ( J:338327 )

♂ • swelling of cardiac mitochondrial ultrastructure is observed after Ang II infusion

muscle

abnormal myocardial fiber mitochondrial morphology ( J:338327 )

♂ • TEM analysis revealed damaged cardiac mitochondrial ultrastructure in cardiomyocytes

increased myocardial fiber size ( J:338327 )

♂ • H&E and wheat germ agglutinin (WGA) staining showed an increase in cardiomyocyte cross sectional area

myocardial fiber disarray ( J:338327 )

♂ • TEM analysis showed a disordered arrangement of myofilaments in cardiomyocytes

myocardium hypertrophy ( J:338327 )

♂

decreased cardiac muscle contractility ( J:338327 )

♂ • at 4 weeks after angiotensin II (Ang II) infusion, mice show a significant decline in the ejection fraction (EF%) and percent fractional shortening (FS%) relative to Ang II-treated wild-type controls, suggesting the decompensated period of cardiac function after Ang II infusion

increased cardiac muscle contractility ( J:338327 )

♂ • in the basal state, hypertrophic hearts exhibit a marked increase in the ejection fraction (EF%) and percent fractional shortening (FS%), likely due to the maintenance or even increased cardiac function during the compensatory stage of cardiac hypertrophy

growth/size/body

enlarged heart ( J:338327 )

♂ • male mice show enlarged hearts at 8 weeks of age

cardiac hypertrophy ( J:338327 )

♂ • at 8 weeks of age, the heart weight to body weight (HW/BW) ratio and the heart weight to tibia length (HW/TL) are both significantly increased, indicating cardiac hypertrophy

♂ • mRNA and protein levels of Nppa (natriuretic peptide type A, also known as ANP) are significantly increased in heart tissue

myocardium hypertrophy ( J:338327 )

♂