Phenotypes associated with this allele
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hey2tm1Gess mutation
(0 available);
any
Hey2 mutation
(30 available)
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Ventricular and atrial septal defects in Hey2tm1Gess/Hey2tm1Gess mice
mortality/aging
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• Background Sensitivity: 80-90% die within 10 days after birth, unlike on a CD-1 background in which lethality rates are much lower
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cardiovascular system
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• Background Sensitivity: exhibit more severe cardiac defects on the C57BL/6 background than on a CD-1 background
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• 8 of 15 at E13.5-E16.5 lack an open connection between the right atrium and ventricle, although the leaflets of the tricuspid valve are formed
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• show persistent foramen ovale
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• Background Sensitivity: ventricular septal defects are much more severe than on a CD-1 background
• high incidence of ventricular septal defects that are consistently located in the upper membranous part of the ventricular septum, just below the atrioventricular junction
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• the few mice surviving to adulthood show altered heart shapes but no valve or septum defects
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hey2tm1Gess mutation
(0 available);
any
Hey2 mutation
(30 available)
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cardiovascular system
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• atrioventricular canal explants from E9.5 embryos show a strong reduction in the number of fully transformed, elongated mesenchymal cells indicating impaired epithelial to mesenchymal transition
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• at E15.5, all mice show a ventricular membranous septal defect very similar to that in Heyltm1Gess Hey1tm1Gess double homozygous mice
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hey2tm1Gess mutation
(0 available);
any
Hey2 mutation
(30 available)
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mortality/aging
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• incomplete penetrance; 80% fail to thrive and die by 10 days of age
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cardiovascular system
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• only identified in higher C57BL/6 backcross generations
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• only identified in higher C57BL/6 backcross generations
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• 30-300% increase in heart to body weight ratios
• normal aorta, however, with normal diameter and no evidence of stenosis or atresia
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growth/size/body
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• 30-300% increase in heart to body weight ratios
• normal aorta, however, with normal diameter and no evidence of stenosis or atresia
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• failure to thrive within the first 10 days of life
• progeny that survive to weaning gradually reach normal body weight by 2-3 mo
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muscle
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hey2tm1Gess mutation
(0 available);
any
Hey2 mutation
(30 available)
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Ventricular and atrial septal defects in Hey2tm1Gess/Hey2tm1Gess mice
mortality/aging
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• Background Sensitivity: lethality rates are much lower than in the C57BL/6 background, and in higher backcross generations almost all homozygotes survive
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cardiovascular system
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• Background Sensitivity: 55.6% of embryos at E16.5 show ventricular septal defects, much less than on a CD-1 background, and do not show any other cardiac defects
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hey1tm1Gess mutation
(0 available);
any
Hey1 mutation
(17 available)
Hey2tm1Gess mutation
(0 available);
any
Hey2 mutation
(30 available)
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mortality/aging
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• by P21 - P28 far fewer mutants are found than expected
• adult mutants also display additional adult lethality from an unknown caus
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hey1tm1Gess mutation
(0 available);
any
Hey1 mutation
(17 available)
Hey2tm1Gess mutation
(0 available);
any
Hey2 mutation
(30 available)
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mortality/aging
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• embryonic survival is reduced by 60% compared to wild-type of Hey1tm1Gess homozygous littermates
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Find Mice |
Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hey1tm1Gess mutation
(0 available);
any
Hey1 mutation
(17 available)
Hey2tm1Gess mutation
(0 available);
any
Hey2 mutation
(30 available)
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mortality/aging
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• no double homozygous embryos survive and all show abnormalities by E10.5
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cardiovascular system
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• reduction in expression of arterial specific markers suggests impaired arterial cell fate specification in double homozygotes
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• the dorsal aortae are frequently reduced or missing on one or both sides of double homozygous embryos probably as a result of impaired aortic wall formation
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• intersomitic vessels formed by angiogenetic sprouting do form but appear less organized than in controls
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• at E10.5 no embryonic blood vessels can be detected in the labyrinthine layer
• however, embryonic vessels are seen in the allantois and chorionic plate
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• the cardinal veins are frequently reduced or missing on one or both sides of double homozygous embryos
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• vascular patterning is coarse especially in the head with many truncated vessels without finely branched trees
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• at E9.5 the heart lacks trabeculae
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• at E9.5 the heart has initiated looping but the myocardium is much thinner
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• at E9.5 - E10.5 the ventricular portion of the heart does not fully enlarge however contractions and blood circulation appear to occur
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• at E10.5 balloon like pericardial sacs are seen in homozygous mutants
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• at E9.5 evidence of hemorrhage can be seen
• at E10.5 massive hemorrhage is seen in the head, trunk, and pericardial cavity of homozygous mutants
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embryo
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• at E9.5 double homozygous embryos appear developmentally retarded
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• at E9.5 the neural tube is thinner and the surrounding mesenchymal cells appear sparse
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• somite formation ceases after E9.5 after 21-26 somites although the somites that do form are normal in size and shape
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• at E10.5 the labyrinthine layer lacks fetal blood circulation and appears very cell-rich without the intermingling of maternal and embryonic blood spaces seen in controls
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• at E10.5 no embryonic blood vessels can be detected in the labyrinthine layer
• however, embryonic vessels are seen in the allantois and chorionic plate
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• formation of an umbilical cord is initiated; however, after E9.5 the connection between embryo and placenta does not mature into a thicker umbilical cord
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• at E9.5 the primitive vascular plexus is present but fails to remodel and by E10.5 is unchanged or degenerating
• by E11.5 when most double homozygous embryos are necrotic no vasculature is left in the yolk sac
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muscle
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• at E9.5 the heart lacks trabeculae
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• at E9.5 the heart has initiated looping but the myocardium is much thinner
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nervous system
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• at E9.5 the neural tube is thinner and the surrounding mesenchymal cells appear sparse
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growth/size/body
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• at E9.5 double homozygous embryos appear developmentally retarded
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