Analysis Tools|
Allele Symbol Allele Name Allele ID |
Nr2f2tm2.1Tsa targeted mutation 2.1, Sophia Y Tsai MGI:3579117 |
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| Summary |
13 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• die by E12
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• thin and well-dilated vessels at E11.5, however did not observe the collapsed or missing anterior cardinal veins displayed by Nr2f2 null mice
• cell layers that separated the artery and vein were greatly reduced at E11.5
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• observed budding hematopoietic cell clusters within veins in several regions, including the head vein, the cardinal vein, and the umbilical vein and veins expressed arterial markers Nrp1 (NP-1) and Notch signaling molecules, that were never observed in wildtype veins, suggesting that veins acquire arterial characteristics
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• exhibit widespread hemorrhage at E11.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• embryos exposed to tamoxifen at E10.5-12.5 show some blood-filled dermal lymphatic vessels
• embryos exposed to tamoxifen show reduced number of superficial vessels (X-gal stained); severity of reduction increases with early tamoxifen treatment
• tamoxifen treatment at E10.5 or E11.5 results in severely reduced lymphatic endothelial cell numbers and lack of lymphatic vessels
• embryos exposed to tamoxifen at E10.5 or 11.5 display drastically mispatterned lymph sacs that are reduced in size compared to controls
• when tamoxifen exposure occurs at E13.5, few embryos show any lymphatic defects, while exposure later in development or postnatally causes no obvious defects despite reduction in Nr2f2 expression in LECs
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• due to defective embryo attachment and decidualization
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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N |
• uterus defects observed in Nr2f2tm2.1Tsa/Nr2f2tm2.1Tsa Pgrtm2(cre)Lyd/Pgr+ mice are rescued
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• at E10.0, number of Prox1+ve lymphatic endothelial cells is dramatically reduced
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• fewer embryos than expected are found at E10.0
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• at E10.0, number of Prox1+ve lymphatic endothelial cells is dramatically reduced
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• not detected at E14.5
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• at E11.5 and E14.5 expression analysis indicates that proximo-ventral cells in the presumptive retinal pigment epithelium possess neural retinal identity
• however, nasal-dorsal cells retain their retinal pigment epithelium identity
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• at E11.5 expression analysis indicates that progenitor cells in the distal ventral optic stalk gain a neural retinal identity
• at E14.5 a neural retina like structure connects directly with the diencephalon
• at E14.5 expression analysis indicates that proximo-ventral cells in the presumptive retinal pigment epithelium possess neural retinal identity
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• at E10.5 the optic stalk resembles the early (E9.5) optic vesicle
• at E12.5 and E14.5 the optic stalk is open ventrally
• the ventral optic stalk is not detected by morphology at E14.5
• however, expression analysis indicates optic stalk identity is maintained but that the boundary between the stalk and neural retina is shifted proximally
• expression analysis indicates that differentiation of dorsal optic stalk cells is impaired
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• seen at E14.5 and persists through birth
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• not detected at E14.5
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• at E11.5 and E14.5 expression analysis indicates that proximo-ventral cells in the presumptive retinal pigment epithelium possess neural retinal identity
• however, nasal-dorsal cells retain their retinal pigment epithelium identity
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• only ~7% of mutant mice are born, indicating embryonic lethality probably due to vascular and heart anomalies resulting from ectopic cre expression
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• by day 10 of pregnancy, formation of fetal blood vessels from the allantois is clearly absent
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• at day 9 of pregnancy, but nor earlier, secondary TGC differentiation appears to increase because more cells are present
• by day 10 of pregnancy, many layers of secondary TGC are noted in mutant females relative to control animals
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• at day 9 of pregnancy, the mutant uterus displays a reduced number of decidual sites with the absence of embryo or the presence of growth-retarded embryos
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• by day 10 of pregnancy, mutant placentas show a reduction in spongiotrophoblast cell number relative to wild-type placentas
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• by day 10 of pregnancy, the mutant labyrinth fails to develop
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• at day 9 of pregnancy, but nor earlier, abnormal placenta development and frequent hemorrhages are observed
• by day 10 of pregnancy, the mutant labyrinth fails to develop
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• mutant females display vaginal bleeding 10-12 days after the presence of a copulatory plug
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• at day 9 of pregnancy, the mutant uterus displays a reduced number of decidual sites with the absence of embryo or the presence of growth-retarded embryos
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• the circular smooth muscle layer of mutant uteri appears disorganized relative to that of wild-type uteri, as shown by anti-smooth muscle actin immunostaining
• in contrast, the mutant endometrium appears relatively normal
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• mutant uterine horns appear shorter than those of control mice
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• upon mating with wild-type males, mutant females exhibit a significant lower number of implantation sites per pregnant female than control females (5.3 2.4 vs 8.8 2.2, respectively)
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• upon mating with wild-type males, mutant females display vaginal bleeding 10-12 days after the presence of a copulatory plug, indicating failure to maintain pregnancy
• at day 9 of pregnancy, most embryos are reabsorbed and a few are growth-retarded
• however, production of endogenous estradiol and progesterone remains unaffected in mutant females
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• despite normal ovarian histology and function, mutant female mice receiving a wild-type ovary are unable to produce pups as observed before ovary transfer
• only 1 of 6 mutant females with wild-type ovaries gave birth to one pup in a 6-month period whereas wild-type females carrying mutant ovaries exhibited normal litter sizes with pups derived from the donor ovary
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• by day 10 of pregnancy, formation of fetal blood vessels from the allantois is clearly absent
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• mutant embryos with hemorrhage are observed
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• mutant females display vaginal bleeding 10-12 days after the presence of a copulatory plug
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• altered radial patterning and anterior-posterior axis patterning of the stomach
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• mesenchyme of the stomach was thickened at E16.5
• hind-stomach was expanded and exhibited a vacuolated epithelium, resembling the pyloric region, with numerous invaginations and a thickened and disorganized circular smooth muscle layer
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• reduced size of fore-stomach as indicated by an anterior shift of the limiting ridge
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• an anterior shift of the limiting ridge is observed
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• the pylorus exhibited a disorganized thickened circular smooth muscle layer, with an epithelium that resembled the epithelium of the duodenum and was devoid of vacuoles, unlike the highly vacuolated control
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• number of parietal cells increased in the thickened epithelial layer at E18.5
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• thicker epithelium at E12.5, E13.5 and E18.5
• the fore-stomach epithelium did not show signs of stratification at E16.5 and resembled hind-stomach epithelium, indicating posteriorization of stomach
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• thicker glandular epithelium at E16.5, however differentiation of this epithelium was unchanged
• exhibited more extensive invagination of the epithelium than in controls
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• the circular smooth muscle layer of the stomach was disorganized at E13.5, E14.5 and E15.5 and was thickened in both the fore-stomach and hind-stomach, suggesting that radial patterning of the stomach was perturbed
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• slightly smaller stomach at E12.5 than controls
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• expansion of enteric neurons in the stomach
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• the circular smooth muscle layer of the stomach was disorganized at E13.5, E14.5 and E15.5 and was thickened in both the fore-stomach and hind-stomach, suggesting that radial patterning of the stomach was perturbed
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• number of parietal cells increased in the thickened epithelial layer at E18.5
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| congenital diaphragmatic hernia | DOID:3827 |
OMIM:142340 OMIM:222400 OMIM:610187 |
J:103437 | |
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 12/10/2024 MGI 6.24 |
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