Phenotypes associated with this allele

• Allele Symbol: Mirc55^tm1.1Eno
• Allele Name: targeted mutation 1.1, Eric N Olson
• Allele ID: MGI:3809690
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Mirc55^tm1.1Eno/Mirc55^tm1.1Eno	Not Specified	MGI:3809702

Genotype
MGI:3809702

hm1

• Allelic Composition: Mirc55^tm1.1Eno/Mirc55^tm1.1Eno
• Genetic Background: Not Specified

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

mortality/aging

increased susceptibility to induced morbidity/mortality ( J:139708 )

• nearly all mice subjected to myocardial infarction die with ventricular rupture compared to only 30% of similarly treated wild-type mice

neonatal lethality, incomplete penetrance ( J:139708 )

• 12% of mice that are born die by P1

postnatal lethality, incomplete penetrance ( J:139708 )

• fewer than expected mice are present at P10 (16% homozygotes compared to the expected 25%)

cellular

decreased vascular endothelial cell proliferation ( J:139708 )

• mice exhibit decreased proliferation of PECAM+ endothelial vascular cells compared to in wild-type mice

reproductive system

reduced female fertility ( J:139708 )

♀

cardiovascular system

abnormal vascular endothelial cell morphology ( J:139708 )

• mice exhibit a lack of endothelial integrity with extensive blood vessel rupturing and a lack of tight cell-cell interaction

abnormal retina vasculature morphology ( J:139708 )

• delayed at P0

abnormal vascular development ( J:139708 )

• at E10.5, cranial vessels fail to grow

• embryonic vasculature is abnormal at E13.5 and E15.5

• retinal vasculature development at P0 is delayed

decreased angiogenesis ( J:139708 )

• endothelial outgrowth of aortic rings is impaired in culture

• the angiogenic response of vascular endothelial cells to Fgf2 is reduced compared to that of wild-type cells

• mice fail to exhibit neovascularization following myocardial infarction unlike wild-type mice

hemorrhage ( J:139708 )

• at E15.5, mice exhibit multifocal hemorrhages and ruptured blood vessels

• at birth, some mice exhibit hemorrhages in the thoracic cavity outside of the pericardial space

abnormal response to cardiac infarction ( J:139708 )

• mice subjected to myocardial infarction exhibit increased ventricular dilation, fibrosis and more extensive loss of functional myocardium compared to in wild-type mice in addition to commonly developing atrial thrombi indicative of heart failure

• mice subjected to myocardial infarction die with ventricular rupture unlike wild-type mice

• mice fail to exhibit neovascularization following myocardial infarction unlike wild-type mice

decreased vascular endothelial cell proliferation ( J:139708 )

• mice exhibit decreased proliferation of PECAM+ endothelial vascular cells compared to in wild-type mice

respiratory system

abnormal lung development ( J:139708 )

• the lungs of mice that die shortly after birth are not inflated

vision/eye

abnormal retina vasculature morphology ( J:139708 )

• delayed at P0

hematopoietic system

increased erythrocyte cell number ( J:139708 )

• in the dermis and liver

homeostasis/metabolism

abnormal response to cardiac infarction ( J:139708 )

• mice subjected to myocardial infarction exhibit increased ventricular dilation, fibrosis and more extensive loss of functional myocardium compared to in wild-type mice in addition to commonly developing atrial thrombi indicative of heart failure

• mice subjected to myocardial infarction die with ventricular rupture unlike wild-type mice

• mice fail to exhibit neovascularization following myocardial infarction unlike wild-type mice

edema ( J:139708 )

• at E15.5, mice exhibit systemic edema

• at birth, some mice exhibit edema in the thoracic cavity outside of the pericardial space

• mice that die shortly after birth exhibit edema

integument

thick dermal layer ( J:139708 )

• at birth, the dermis is thickened with erythrocytes in the tissue spaces