Phenotypes associated with this allele
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hand1tm1Eno mutation
(1 available);
any
Hand1 mutation
(14 available)
Hand1tm2Eno mutation
(0 available);
any
Hand1 mutation
(14 available)
Rr133tm1Eno mutation
(0 available);
any
Rr133 mutation
(0 available)
Tg(Nkx2-5-cre)9Eno mutation
(0 available)
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mortality/aging
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• no mutant embryos are found after E10.5
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cardiovascular system
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• at E10.5 the myocardium is poorly trabeculated
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• at E10.5 the myocardium is thin
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embryo
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• at E10.5 mutant embryos appear slightly delayed compared to compound heterozygotes lacking only Hand1
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muscle
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• at E10.5 the myocardium is poorly trabeculated
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• at E10.5 the myocardium is thin
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growth/size/body
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• at E10.5 mutant embryos appear slightly delayed compared to compound heterozygotes lacking only Hand1
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hand1tm1Eno mutation
(1 available);
any
Hand1 mutation
(14 available)
Hand1tm2Eno mutation
(0 available);
any
Hand1 mutation
(14 available)
Rr133tm1Eno mutation
(0 available);
any
Rr133 mutation
(0 available)
Tg(Nkx2-5-cre)9Eno mutation
(0 available)
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mortality/aging
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• no mutant embryos are found after E9.0
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cardiovascular system
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• at E9.0 some segments of the myocardial wall contain cells that resemble mesenchymal cells rather than cardiomyocytes
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• at E9.0 only a single atrium is present
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• at E9.0 only a single immature ventricle is present and the lumen of the ventricle is abnormally narrow
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muscle
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• at E9.0 some segments of the myocardial wall contain cells that resemble mesenchymal cells rather than cardiomyocytes
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hand1tm1Eno mutation
(1 available);
any
Hand1 mutation
(14 available)
Hand1tm2Eno mutation
(0 available);
any
Hand1 mutation
(14 available)
Tg(Nkx2-5-cre)9Eno mutation
(0 available)
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mortality/aging
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• most mutants die within 2-4 days of birth
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cardiovascular system
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• heart defects similar to those seen in compound heterozygotes hemizygous for Tg(Myhca-cre)2182Mds are found
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hand2tm1Dsr mutation
(0 available);
any
Hand2 mutation
(12 available)
Hand2tm2.1Dsr mutation
(0 available);
any
Hand2 mutation
(12 available)
Tg(Nkx2-5-cre)9Eno mutation
(0 available)
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mortality/aging
cardiovascular system
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gata4tm1.1Wtp mutation
(0 available);
any
Gata4 mutation
(36 available)
Gata4tm1Grg mutation
(1 available);
any
Gata4 mutation
(36 available)
Tg(Nkx2-5-cre)9Eno mutation
(0 available)
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Growth retardation and myocardial thinning in Gata4tm1.1Wtp/Gata4tm1Grg Tg(Nkx2-5-cre)9Eno/0 mice
mortality/aging
growth/size/body
cardiovascular system
embryo
muscle
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Syne1tm1Chen mutation
(0 available);
any
Syne1 mutation
(202 available)
Syne2tm1.1Chen mutation
(0 available);
any
Syne2 mutation
(297 available)
Tg(Nkx2-5-cre)9Eno mutation
(0 available)
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Ultrastructural nuclear abnormalities in Syne1tm1Chen/Syne1tm1Chen Syne2tm1.1ChenSyne2tm1.1Chen Tg(Nkx2-5-cre)9Eno/? cardiomyocytes
cardiovascular system
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N |
• heart rate remains unchanged through course of study
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• significant increase in heart weight/body weight and heart weight/total length ratios at 10 weeks of age
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• wall thinning observed at 10 weeks but not at 5 weeks of age
• thinning continues through 25 and 52 weeks
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• diminished fractional shortening at 10 weeks but not 5 weeks of age
• fractional shortening continues to decline at 25 and 52 weeks
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cellular
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• nuclei are considerably enlarged and binuclei are closer together
• nuclei are less circular
• nuclear abnormalities begin to appear at 1 day of age
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muscle
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• diminished fractional shortening at 10 weeks but not 5 weeks of age
• fractional shortening continues to decline at 25 and 52 weeks
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Syne1tm1Chen mutation
(0 available);
any
Syne1 mutation
(202 available)
Tg(Nkx2-5-cre)9Eno mutation
(0 available)
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cellular
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• nuclei are enlarged
• nuclei are less circular
• nuclei are closer together in binuclear cardiomyocytes
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nkx2-5-cre)9Eno mutation
(0 available)
Tmsb4xtm1.2Chen mutation
(0 available);
any
Tmsb4x mutation
(11 available)
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normal phenotype
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• mutant mice are viable to adulthood
• mice did not have alterations in heart weight/body weight or heart weight/ tibia length compared with control mice
• histological observations as well as expression of fetal gene and fibrotic markers were also similar to control mice
• mice have normal cardiac function, chamber size, and wall thickness compared with their littermate controls
• no changes in vessel volume in mutant mice
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Rac1tm1Djk mutation
(1 available);
any
Rac1 mutation
(21 available)
Tg(Nkx2-5-cre)9Eno mutation
(0 available)
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mortality/aging
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• although mice are alive from E11.5 to E18.5, all neonates are found dead at P0
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cardiovascular system
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• at E14.5-P0, hearts exhibit impaired alignment of the outflow tract (OFT) to the ventricles
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• at E14.5-P0, all (17 of 17) hearts display more than one type of congenital heart defect (CHD), not observed in control hearts
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• at E15.5, the compact myocardium of both ventricles is poorly formed
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• at E14.5-P0, all hearts (17 of 17) exhibit a thin compact myocardium
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• at E15.5, both the left ventricle (LV) and right ventricle (RV) show a significant decrease in compact myocardium thickness relative to controls
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• at E18.5, the ventricular myocardium shows severe disruption of F-actin filament organization
• at E9.5, the cell proliferation rate in the ventricular myocardium is significantly lower than in control hearts, as assessed by the percentage of pHH3+ and cyclin D1+ cardiomyocytes
• however, no aberrant apoptosis is detected in the ventricular myocardium at E9.5
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• at E15.5, both the left ventricle (LV) and right ventricle (RV) show hypertrabeculation; the trabecular to compact myocardium ratio is increased by >2.5-fold relative to controls
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• at E12.5, mRNA expression of Scrib and other cardiac transcription and growth factors (Nkx2.5, Gata4, Tbx5, Tbx20, Hand1, Hand2 and Bmp10) is significantly decreased relative to control hearts
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• at E18.5, cardiomyocytes in the ventricular myocardium exhibit a rounded morphology and appear highly disorganized in both the RV and LV while the short axis of cardiomyocyte diameter is significantly larger than in controls, indicating impaired cardiomyocyte polarization and elongation
• at E15.5, overall expression of SCRIB (scribble planar cell polarity protein) is significantly reduced in the myocardium surrounding the aorta (OFT), RV and LV, supporting a failure of cardiomyocytes to undergo polarization
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• at E14.5-P0, 64.7% (11 of 17) hearts exhibit DORV: both pulmonary artery and aorta are connected to the right ventricle
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• at E14.5-P0, 35.3% (6 of 17) hearts exhibit and overriding aorta
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• at E14.5-P0, all (17 of 17) hearts show a bifid cardiac apex (a bifurcation between the right and the left ventricle)
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• at E14.5-P0, all hearts (17 of 17) show ventricular septal defects
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• at E9.5, the cell proliferation rate in the ventricular myocardium is significantly lower than in control hearts, as assessed by the percentage of pHH3+ and cyclin D1+ cardiomyocytes
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cellular
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• at E9.5, the cell proliferation rate in the ventricular myocardium is significantly lower than in control hearts, as assessed by the percentage of pHH3+ and cyclin D1+ cardiomyocytes
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muscle
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• at E15.5, the compact myocardium of both ventricles is poorly formed
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• at E14.5-P0, all hearts (17 of 17) exhibit a thin compact myocardium
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• at E15.5, both the left ventricle (LV) and right ventricle (RV) show a significant decrease in compact myocardium thickness relative to controls
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• at E18.5, the ventricular myocardium shows severe disruption of F-actin filament organization
• at E9.5, the cell proliferation rate in the ventricular myocardium is significantly lower than in control hearts, as assessed by the percentage of pHH3+ and cyclin D1+ cardiomyocytes
• however, no aberrant apoptosis is detected in the ventricular myocardium at E9.5
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• at E15.5, both the left ventricle (LV) and right ventricle (RV) show hypertrabeculation; the trabecular to compact myocardium ratio is increased by >2.5-fold relative to controls
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• at E9.5, the cell proliferation rate in the ventricular myocardium is significantly lower than in control hearts, as assessed by the percentage of pHH3+ and cyclin D1+ cardiomyocytes
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hey2tm1Eno mutation
(1 available);
any
Hey2 mutation
(30 available)
Hey2tm2Eno mutation
(0 available);
any
Hey2 mutation
(30 available)
Tg(Nkx2-5-cre)9Eno mutation
(0 available)
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cardiovascular system
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• adult mice have grossly enlarged hearts
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• base of dilated right ventricle merges with interventricular septum above apex of heart; this is apparent by E13.5 and persists in adults
• at 6 weeks of age, ectopic activation of atrial regular and structural genes (>10-fold greater than wild-type littermates) is observed in ventricular myocardium
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• VSDs are not observed in all mice, however, some show VSDs or delay of ventricular septal formation at E13.5-17.5
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• at 6 weeks of age, mice show an increase in systolic left ventricular internal diameter (LVID)
• normal diastolic left ventricular internal diameter does not change significantly relative to wild-type
• atrial naturietic factor (ANF) and Tbx5 expression is increased in left ventricle at E17.5, whereas expression is seen in atria and trabecular cells in wild-type
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• deterioration in heart contractility, accompanied by decreased fractional shortening (FS)
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muscle
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• deterioration in heart contractility, accompanied by decreased fractional shortening (FS)
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growth/size/body
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• adult mice have grossly enlarged hearts
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Nkx2-5-cre)9Eno mutation
(0 available)
Zswim8em2Jtm mutation
(1 available);
any
Zswim8 mutation
(52 available)
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mortality/aging
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N |
• unlike germline null mice, conditional loss in hear progenitor cells does not result i neonatal lethality
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cardiovascular system
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• apex is less distinct
• cardiac phenotypes are less severe than in germline null mice
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Commd9tm1c(KOMP)Wtsi mutation
(0 available);
any
Commd9 mutation
(49 available)
Tg(Nkx2-5-cre)9Eno mutation
(0 available)
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mortality/aging
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• only 14% (versus expected 25%) of mice are viable at birth; time of lethality is not specified
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| Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Irx3tm3Hui mutation
(0 available);
any
Irx3 mutation
(24 available)
Irx5tm3Hui mutation
(0 available);
any
Irx5 mutation
(30 available)
Tg(Nkx2-5-cre)9Eno mutation
(0 available)
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cardiovascular system
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N |
• no defects in heart morphology are detected
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Analysis Tools