Analysis Tools|
Allele Symbol Allele Name Allele ID |
Tg(Tie1-cre)9Ref transgene insertion 9, Reinhard Fassler MGI:2385916 |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Summary |
15 genotypes
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• embryonic lethality at mid gestation
|
|
• develop similar yolk sac defects as Tgfbr1 null mice
|
|
• develop similar yolk sac defects as Tgfbr1 null mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice are present at E9.5 but dead by E12.5
|
|
• at E9.5
|
|
• mice lack networks of vessels at all stages
|
|
• at E9.5
|
|
• at E9.5, mice appear delayed by 1 day
|
|
• at E9.5, mice appear delayed by 1 day
|
|
• at E9.5
|
|
• at E9.5
|
|
• mice lack networks of vessels at all stages
|
|
• at E9.5, hearts exhibit pericardial effusion
|
|
• at E9.5, hearts exhibit pericardial effusion
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice are present at E9.5 but dead by E12.5
|
|
• at E9.5
|
|
• mice lack networks of vessels at all stages
|
|
• at E9.5, mice appear delayed by 1 day
|
|
• yolk sacs possess greater numbers of vascular smooth muscle cells than in wild-type yolk sacs
|
|
• at E9.5, mice appear delayed by 1 day
|
|
• at E9.5
|
|
• mice lack networks of vessels at all stages
|
|
• at E9.5, hearts exhibit pericardial effusion
|
|
• at E9.5, hearts exhibit pericardial effusion
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• thin myocardium is seen at E18.5, however this abnormality is normalized by 1 month of age
|
|
• E15.5 embryos show irregular capillary diameter with microaneurysms in the brain
• capillaries in the striatum with associated pericytes are straighter and more uniform in diameter
• in the cerebellum, see a reduction of capillary density in the gray matter and the presence of numerous enlarged capillaries
|
|
• in the striatum, capillary density is lower, but numerous tortuous capillaries with increased diameter are seen in capillary regions not associated with pericytes
• in the cerebellum, see a reduction of capillary density in the gray matter and the presence of numerous enlarged capillaries
|
|
• E18.5 glomeruli show dilation of the remaining capillary loops
• 3-week old mutants show an increase in the diameter of individual capillary loops
|
|
• in the striatum, capillary density is lower, but numerous tortuous capillaries with increased diameter are seen in capillary regions not associated with pericytes
|
|
• microaneurysm formation in the brain
|
|
• in mutants with greater than 50% of normal overall CNS pericyte density, the retinal vasculature displays irregular microvessel diameter, microaneurysms, and increased vascular regression
• in mutants with less than 50% of normal pericyte density, the retinas develop regions with massive increase of abnormal vessels extending into the vitreous and choroid
|
|
• exhibit a variable reduction in pericyte density in CNS vessels, affecting arteries, veins and capillaries
(J:78544)
• retinas in mutants with the lowest overall CNS pericyte density however display focal regions of increased pericyte density
(J:78544)
• exhibit a significant reduction in pericyte density in E15.5 embryos that persists into adulthood
(J:89186)
|
|
• placental defects at E18.5 include dilation of both fetal and maternal vessels due to a reduction in the number of pericytes and trophoblasts
|
|
• thin myocardium is seen at E18.5, however this abnormality is normalized by 1 month of age
|
|
• show scattered small hemorrhages deep in the cerebral parenchyma; bleeding seems to start from capillary branching points
|
|
• mutants with less than 52% of the normal pericyte density in the cerebellum show typical hallmarks of proliferative retinopathy, affecting at least one eye
• retinas of mutants with the lowest overall CNS pericyte density are contracted and often attached to the retinal pigment epithelial cells and the lens
|
|
• in mutants with greater than 50% of normal overall CNS pericyte density, the retinal vasculature displays irregular microvessel diameter, microaneurysms, and increased vascular regression
• in mutants with less than 50% of normal pericyte density, the retinas develop regions with massive increase of abnormal vessels extending into the vitreous and choroid
|
|
• regions with high pericyte density show loss of organization of the neural layers and folding of the photoreceptor layer producing typical photoreceptor rosette profiles
|
|
• placental defects at E18.5 include dilation of both fetal and maternal vessels due to a reduction in the number of pericytes and trophoblasts
|
|
• mutants older than 12 months develop mild but significant increases in albumin content in urine
|
|
• microaneurysm formation in the brain
|
|
• show scattered small hemorrhages deep in the cerebral parenchyma; bleeding seems to start from capillary branching points
|
|
• postnatal brains show increased density of microglial cells at sites of bleeding
|
|
• postnatal brains show increased density of microglial cells and upregulated expression of glial fibrillary acidic protein at sites of bleeding, hallmarks of reactive gliosis
|
|
• mutants older than 12 months develop mild but significant increases in albumin content in urine
|
|
• E18.5 glomeruli show a reduction in tuft complexity and dilation of the remaining capillary loops
• 3-week old mutants show glomerular dilation, both an increased glomerulus diameter and an increase in the diameter of the individual capillary loops, however by 6 and 21 months of age, no signs of increased glomerular pathology are seen
|
|
• E18.5 glomeruli show dilation of the remaining capillary loops
• 3-week old mutants show an increase in the diameter of individual capillary loops
|
|
• most glomeruli show a reduced mesangial core, although some completely lack mesangial cells at E18.5
• the mesangial deficiency is largely corrected at 3 weeks of age
|
|
• postnatal brains show increased density of microglial cells at sites of bleeding
|
|
• postnatal brains show increased density of microglial cells at sites of bleeding
|
|
• most glomeruli show a reduced mesangial core, although some completely lack mesangial cells at E18.5
• the mesangial deficiency is largely corrected at 3 weeks of age
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• mutants exhibit normal blood vessel development, normal blood vessel morphology in adults, normal angiogenesis, and a similar vascular remodeling response as controls
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• injected cell derived tumors display increased blood vessel density
|
|
• increase in tumor size 10 - 12 days after injection of Lewis lung carcinoma or murine melanoma cells compared to controls
|
|
• injected cell derived tumors display increased blood vessel density
|
|
• increase in vessel growth into implanted VEGF treated sponges and enhanced VEGF induced micro vessel sprouting in vitro compared to controls
• however, vessel density in untreated skin is not different from controls
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• embryonic lethality at mid gestation
|
|
• develop similar yolk sac defects as Tgfbr2 null mice
|
|
• develop similar yolk sac defects as Tgfbr2 null mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• smaller tumors induced by AOM/DSS
• however, development of induced colitis is normal
|
|
• smaller tumors induced by AOM/DSS
• however, development of induced colitis is normal
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• reduced proliferation and increased apoptosis of tumor cells compared to in Apcmin heterozygotes
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• unlike null homozygotes, mice survive to adulthood
|
|
• at E14.5, mice exhibit blood-filled vessels unlike wild-type mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• expected number of mice are produced
|
| N |
• no developmental defects are observed
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice are born healthy and fertile suggesting that the the midgestational
embryonic lethality observed in Elavl1 null mice results from placental
failure due to extraembryonic defects
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• embryos show growth retardation compared to littermate controls at E17.5
|
|
• at E17.5, skin in the head region shows decreased branching and capillary density compared to controls
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• compound heterozygotes die around E12, similar to Casp8tm1.1Yuan homozygotes
|
|
• the density of the vasculature in the yolk sac is decreased
|
|
• severe congestion of the liver and large vessels of the chest and abdomen similar to Casp8tm1.1Yuan homozygotes is seen
|
|
• extensive necrosis of the cardiomyocytes in the ventricles and atria is seen
|
|
• the heart has a globose shape
|
|
• around E12 thin and occasionally ruptured ventricular walls are seen
• heart defects are not seen in mutants at E10-E11.5
|
|
• around E12, the pericardial space is enlarged consistent with pericardial edema
|
|
• extensive necrosis of the cardiomyocytes in the ventricles and atria is seen
|
|
• the density of the vasculature in the yolk sac is decreased
|
|
• an undulated neural tube is seen
|
|
• the density of the vasculature and amount of blood in the yolk sac is decreased
• increased cell death is seen in the yolk sac at E10.5 even when no signs of vascular degeneration were detected
|
| N |
• hematopoietic progenitor numbers are not decreased unlike in Casp8tm1.1Yuan homozygotes
|
|
• around E12, the pericardial space is enlarged consistent with pericardial edema
|
|
• an undulated neural tube is seen
|
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
||
|
Citing These Resources Funding Information Warranty Disclaimer, Privacy Notice, Licensing, & Copyright Send questions and comments to User Support. |
last database update 10/09/2024 MGI 6.24 |
|
|
|
||
