Analysis Tools
normal phenotype
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• homozygous mice exhibit no discernable phenotype; mice are viable and fertile
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Allele Symbol Allele Name Allele ID |
Foxa2tm1Khk targeted mutation 1, Klaus H Kaestner MGI:2177337 |
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| Summary |
12 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• homozygous mice exhibit no discernable phenotype; mice are viable and fertile
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mutant animals die between P9 and P12
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• pancreatic beta cells are present, but have abnormal morphology
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• disorganized morphology with non-beta cells present in the core
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• beta cells exhibit dysregulated insulin secretion
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• mutant animals are smaller than controls at P8
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• beta cells exhibit dysregulated insulin secretion
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• described as severe in mutant animals
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• level was 5 fold less in mutant mice than in control animals
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• the plasma insulin level was very high considering the low glucose levels in mutant animals
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• mutant mice have a 2.5-fold higher glycogen content than controls
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• most mice treated with doxycycline from E0 die on P1
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• 50% of mice treated with doxycycline from E0 through P16 died within 30 days of birth
(J:88601)
• only 46% of mice treated with doxycycline from E0 survive to P5
(J:93473)
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• observed in bronchoalveolar lavage from mice treated with doxycycline from E0 through P16
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• observed in bronchoalveolar lavage from mice treated with doxycycline from E0 through P16
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• observed in bronchoalveolar lavage from mice treated with doxycycline from E0 through P16
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• observed in bronchoalveolar lavage from mice treated with doxycycline from E0 through P16
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• mice treated with doxycycline from E0 and found to be in distress or moribund on P1 display pulmonary congestion
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• impaired alveogenesis marked by fewer peripheral lung saccules and decreased alveolar septation; apparent at 3 days of age in mice treated with doxycycline from E0 through P16
(J:88601)
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• at E18.5, mice treated with doxycycline from E0 display immature peripheral lung saccules, resembling those normally seen at E16-E17
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• at E18.5, squamous type I cells are missing, alveolar walls are thickened and lined by immature cuboidal type II cells, cytoplasmic glycogen is dispersed, and apical microvilli are absent
• however, no evidence of capillary leakage or endothelial cell abnormalities are observed
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• at E18.5, no squamous type I cells are observed in mice treated with doxycycline from E0
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• at E18.5, mice treated with doxycycline from E0 show absence of lamellar bodies in alveolar type II cells
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• at E18.5, mice treated with doxycycline from E0 show thickened alveolar walls lined by immature cuboidal type II cells
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• mice treated with doxycycline from E0 and found to be in distress or moribund on P1 display focal or extensive atelectasis
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• increased airspace in mice prenatally treated with doxycycline
• postnatal treatment with doxycycline also resulted in increased airspace but to a lesser extent
• normal prenatal lung morphogenesis
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• mice treated with doxycycline from E0 and found to be in distress or moribund on P1 display hyaline membrane formation
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• goblet cell hyperplasia, associated with the accumulation of both neutral and acidic mucins, observed in mice treated with doxycycline from E0 through P16
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• ~50% of mice treated with doxycycline from E0 develop severe respiratory distress within 2-3 hrs of birth
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• at E18.5, the fractional content of phosphatidylcholine (PC) and saturated PC are markdely reduced, whereas that of phosphatidylethanolamine, sphingomyelin, and phosphatidylserine is increased in the lungs of mice treated with doxycycline from E0
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• SP-A, SP-B, and SP-C mRNAs are significantly decreased at E18.5
• the active SP-B peptide is markedly decreased in lung homogenates prior to birth
• SP-D mRNAs are significantly increased at E18.5
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• at E18.5, no secreted surfactant is detected in the air spaces of mice treated with doxycycline from E0
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• newborn mice are frequently cannibalized by the mother
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• mice treated with doxycycline from E0 and found to be in distress or moribund on P1 display pulmonary congestion
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice die prior to P5
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• the pancreas occupies 31% relative area compared to in wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• unlike in mice lacking both alleles of Fox2a, pancreatic development is normal
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| N |
• mice are euglycemic
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice die within 2 days of birth
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• the spaces between the remaining ductal epithelia are filled with stromal tissue, including fibroblasts and smooth musce cells
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• very few beta cells are present between E17.5 and P1
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• at E13.5, pancreatic precursor cells fail to expand resulting in fewer than normal glucagon+ and amylase+ cells
• pancreatic development is arrested at the early pancreatic cord stage
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• the pancreas occupies 19% relative area compared to in wild-type mice
• the numbers of endocrine cells, exocrine cells, and total epithelial tissue is severely decreased compared to in wild-type mice with remaining cells exhibiting an almost exclusively ductal phenotype
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• although blastocysts can attach to the uterine lumen and initiate a decidual response, the decidual region and size of the embryos is significantly smaller on day 5.5 of natural pregnancy
• after induction of artificial decidualization, stimulated horn weight:unstimulated horn weight ratio is significantly lower than that in controls
• decidualization defect can be partially rescued by intrauterine injection of recombinant leukemia inhibitory factor (LIF) prior to the initiation of the decidual response
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• uteri of 8-wk-old females show a severe defect in endometrial gland development
• loss of endometrial glands results in a marked reduction of leukemia inhibitory factor (Lif) expression on day 3.5 of pseudopregnancy
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• nonpregnant uteri of 8-wk-old females show a severe reduction in the number of endometrial glands relative to control uteri
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• on day 5.5 of pregnancy, embryos fail to exhibit invasion into the uterine stroma through the epithelium
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• on day 5.5 of pregnancy, the number of implantation sites is significantly lower than that in control uteri
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• uterus is unable to support embryo invasion and undergo an experimentally induced decidual response with exogenous steroid hormones
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• when mated to wild-type males for a period of 6 months, females exhibit severe subfertility, with significantly fewer litters, pups per litter and total pups born relative to control females
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• females produce significantly fewer pups per litter than control females
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• although blastocysts can attach to the uterine lumen and initiate a decidual response, the decidual region and size of the embryos is significantly smaller on day 5.5 of natural pregnancy
• after induction of artificial decidualization, stimulated horn weight:unstimulated horn weight ratio is significantly lower than that in controls
• decidualization defect can be partially rescued by intrauterine injection of recombinant leukemia inhibitory factor (LIF) prior to the initiation of the decidual response
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• uteri of 8-wk-old females show a severe defect in endometrial gland development
• loss of endometrial glands results in a marked reduction of leukemia inhibitory factor (Lif) expression on day 3.5 of pseudopregnancy
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• nonpregnant uteri of 8-wk-old females show a severe reduction in the number of endometrial glands relative to control uteri
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• male mutants injected with DEN followed by TCPOBOP (carcinogen treatment) show reduced tumor growth compared to control males that develop severe hepatocellular carcinoma
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• female mutants injected with DEN followed by TCPOBOP (carcinogen treatment) to induce rapid hepatocellular carcinoma formation, develop multiple and large liver tumors unlike control females that are resistant to hepatocellular carcinoma development
• in females treated with fulverstrant to block estrogen signaling, DEN-induced liver injury is significantly attenuated
• estrogen treatment of male mutants enhances liver injury in DEN-treated males while in DEN-treated controls estrogen treatment prevents liver injury and carcinogenesis
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• female mutants injected with N,N-diethylnitrosamine (DEN) followed by TCPOBOP two-step strategy (carcinogen treatment) to induce rapid hepatocellular carcinoma formation, develop multiple and large liver tumors unlike control females that are resistant to hepatocellular carcinoma development
• male mutants injected with DEN followed by TCPOBOP show reduced tumor growth compared to control males that develop severe hepatocellular carcinoma
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• male mutants injected with DEN followed by TCPOBOP (carcinogen treatment) show reduced tumor growth compared to control males that develop severe hepatocellular carcinoma
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• female mutants injected with DEN followed by TCPOBOP (carcinogen treatment) to induce rapid hepatocellular carcinoma formation, develop multiple and large liver tumors unlike control females that are resistant to hepatocellular carcinoma development
• in females treated with fulverstrant to block estrogen signaling, DEN-induced liver injury is significantly attenuated
• estrogen treatment of male mutants enhances liver injury in DEN-treated males while in DEN-treated controls estrogen treatment prevents liver injury and carcinogenesis
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• female mutants injected with N,N-diethylnitrosamine (DEN) followed by TCPOBOP two-step strategy (carcinogen treatment) to induce rapid hepatocellular carcinoma formation, develop multiple and large liver tumors unlike control females that are resistant to hepatocellular carcinoma development
• male mutants injected with DEN followed by TCPOBOP show reduced tumor growth compared to control males that develop severe hepatocellular carcinoma
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mutant embryos die at E11.5
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• the axial mesendoderm failed to differentiate; the anterior neural plate and anterior definitive endoderm form, but fail to maintain specification
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• anterior head truncations were noted in mutant animals
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• homozygous mice exhibit no discernable phenotype; mice are viable and fertile with normal liver metabolism and normal glucose homeostasis
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• most die by P3, with a few surviving to P5
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• the number of mature glucagon-positive pancreatic alpha-cells is reduced
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• islets are irregularly shaped and display a disorganized architecture with many small clusters of endocrine cells embedded in the exocrine tissue
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• severely hypoglycemic
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• 50% reduction of plasma glucagon
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• no increase in the number of neutrophils or macrophages in mice treated with doxycycline from E0 through P16
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• goblet cell hyperplasia, associated with the accumulation of both neutral and acidic mucins, in the larger airways of mice treated with doxycycline from E0 through P16
• neither airspace nor alveolar morphological abnormalities were detected
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• increased in mice treated with doxycycline
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• decreased in mice treated with doxycycline
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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 04/30/2024 MGI 6.23 |
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