Phenotypes associated with this allele

• Allele Symbol: Tg(Myh6-cre/Esr1*)1Liao
• Allele Name: transgene insertion 1, James K Liao
• Allele ID: MGI:3654324
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
cn1	Rac1^tm1Djk/Rac1^tm1.1Djk Tg(Myh6-cre/Esr1*)1Liao/0	involves: 129S4/SvJae * C57BL/6	MGI:3654330
cn2	Tg(CAG-Calr)#Mlk/0 Tg(Myh6-cre/Esr1*)1Liao/0	involves: C57BL/6	MGI:6108900

Genotype
MGI:3654330

cn1

• Allelic Composition: Rac1^tm1Djk/Rac1^tm1.1Djk; Tg(Myh6-cre/Esr1*)1Liao/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6

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

cellular

oxidative stress ( J:109582 )

• superoxide anion production is reduced in cardiac-specific Rac1-nulls compared to wild-type in response to angiotensin II (increase of 3.3-fold in wild-type, 2.1-fold in heterozygotes and only 1.2 fold in Rac1 nulls)

homeostasis/metabolism

abnormal enzyme/coenzyme activity ( J:109582 )

• ASK1 and NF-kappaB activities are increased in wild-type and to a lesser extent in heterozygotes by angiotensin II, but not at all in null mice

increased NAD(P)H oxidase activity ( J:109582 )

• NADPH oxidase activity is increased to a greater extent in response to angiotensin II in wild-type than in heterozygotes or cardiac-specific Rac1 nulls

cardiovascular system

abnormal myocardium layer morphology ( J:109582 )

• 2 weeks after infusion of angiotensin II, hearts from cardiac-specific Rac1-deletion show reduced end-diastolic myocardial wall thickness

abnormal myocardial fiber morphology ( J:109582 )

• cross-sectional areas of cardiomyocytes in wild-type and Rac1 heterozygotes are increased in response to angiotensin II (300 and 270 um² vs 200 um² in untreated controls) but areas of cardiomyocytes from nulls show no change

cardiac hypertrophy ( J:109582 )

• 2 weeks after infusion of angiotensin II or saline, hearts from cardiac specific Rac1-deletion show less hypertrophy than wild-type or Rac1 heterozygotes

increased heart left ventricle weight ( J:109582 )

• angiotensin II increases left ventricular mass of wild-type and Rac1 heterozygotes by 184 and 160% respectively, while cardiac-specific Rac1 nulls have only a 123% increase

muscle

abnormal myocardium layer morphology ( J:109582 )

• 2 weeks after infusion of angiotensin II, hearts from cardiac-specific Rac1-deletion show reduced end-diastolic myocardial wall thickness

abnormal myocardial fiber morphology ( J:109582 )

• cross-sectional areas of cardiomyocytes in wild-type and Rac1 heterozygotes are increased in response to angiotensin II (300 and 270 um² vs 200 um² in untreated controls) but areas of cardiomyocytes from nulls show no change

growth/size/body

cardiac hypertrophy ( J:109582 )

• 2 weeks after infusion of angiotensin II or saline, hearts from cardiac specific Rac1-deletion show less hypertrophy than wild-type or Rac1 heterozygotes

Genotype
MGI:6108900

cn2

• Allelic Composition: Tg(CAG-Calr)#Mlk/0; Tg(Myh6-cre/Esr1*)1Liao/0
• Genetic Background: involves: C57BL/6

cardiovascular system

enlarged heart ( J:199413 )

• tamoxifen-treated mice exhibit enlarged cardiac chambers

dilated heart left ventricle ( J:199413 )

• as early as 1 week after tamoxifen treatment, less than 30% of mice show dilatation of the left ventricle chamber

• adult hearts of tamoxifen treated mice exhibit enlarged left ventricle chamber with thinned posterior wall

cardiac interstitial fibrosis ( J:253065 )

• tamoxifen-treated mice develop severe cardiac fibrosis

• treatment of tamoxifen-induced mice with TUDCA, the taurine-conjugated form of ursodeoxycholic acid, reduces cardiac fibrosis

dilated cardiomyopathy ( J:199413 )

• in tamoxifen-treated mice

decreased cardiac muscle contractility ( J:199413 )

• as early as 1 week after tamoxifen treatment, less than 30% of mice show reduced percent ejection fraction

abnormal heart echocardiography feature ( J:199413 )

• echocardiography of tamoxifen-induced mice indicates severe left ventricle dilation, increase in left ventricle internal dimension, decreased systolic function of the left ventricle, and increased Tci index of the left ventricle, an indicator of systolic and diastolic function, prolongation of the isovolumic intervals and shortening of ejection fraction

abnormal heart electrocardiography waveform feature ( J:199413 )

• absence of A-wave indicating a restricted pattern of transmitral flow velocity

prolonged PR interval ( J:199413 )

• tamoxifen-treated mice show a longer PR interval indicating prolonged AV conduction

abnormal P wave ( J:199413 )

• P wave amplitude as a proportion of the QRS amplitude is increased in tamoxifen-treated mice

decreased QRS amplitude ( J:199413 )

• QRS amplitude is reduced in tamoxifen-treated mice

abnormal T wave ( J:199413 )

• tamoxifen-treated mice exhibit a weak T amplitude of electrical impulse

congestive heart failure ( J:199413 )

• in tamoxifen-treated mice

growth/size/body

enlarged heart ( J:199413 )

• tamoxifen-treated mice exhibit enlarged cardiac chambers

decreased body weight ( J:199413 )

• in tamoxifen-treated mice

muscle

dilated cardiomyopathy ( J:199413 )

• in tamoxifen-treated mice

decreased cardiac muscle contractility ( J:199413 )

• as early as 1 week after tamoxifen treatment, less than 30% of mice show reduced percent ejection fraction

cellular

cardiac interstitial fibrosis ( J:253065 )

• tamoxifen-treated mice develop severe cardiac fibrosis

• treatment of tamoxifen-induced mice with TUDCA, the taurine-conjugated form of ursodeoxycholic acid, reduces cardiac fibrosis

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
congestive heart failure		DOID:6000		J:253065