Analysis Tools|
Allele Symbol Allele Name Allele ID |
Espl1+ wild type MGI:2441242 |
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| Summary |
8 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• longer mean average tumor free lifespan (more than 800 days vs. 600 days for wild-type)
• no tumors are observed during the lifespan of mice compared to about 5% tumor incidence in wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following Cre-adenovirus treatment, mouse embryonic fibroblast sister chromatids fail to separate at the centromere
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• treatment with Cre-adenovirus severely restricts proliferation of mouse embryonic fibroblast cells
• however, there is no accumulation of DNA as seen in Espl1tm1.1Tno/ Espl1tm1.2Tno mice following Cre-adenovirus treatment
• however, infection with Cre-adenovirus can reduce some growth in the absence of floxed alleles
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• lack spermatogonia
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• lack of primordial germ cells by E14.5 (early germ cell marker Mvh absent)
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• primordial germ cells migrate to genital ridge but fail to proliferate normally between 11.5 and 14.5 dpc
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• significantly smaller testes at 6 wks of age
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• no sign of spermatogenesis detected at 2 wks of age, due to spermatogonia cell depletion
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• absence of spermatids in seminiferous tubules
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• absence of spermatocytes in seminiferous tubules
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• both sexes are sterile
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• absence of spermatids in seminiferous tubules
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• absence of spermatocytes in seminiferous tubules
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• lack spermatogonia
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• lack of primordial germ cells by E14.5 (early germ cell marker Mvh absent)
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• abnormal centrosome number (>2) in some mutant PGCs at 13.5 dpc
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• abnormal centrosome number (>2) in some mutant PGCs at 13.5 dpc
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• abnormal metaphase configuration of mutant PGCs at 13.5 dpc
• precocious sister chromatid separation and arrest of PGCs in mitosis due to spindle checkpoint activation
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• significantly higher mitotic indices in mutant PGCs than controls at 12.5, 13.5, and 14.5 dpc
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• primordial germ cells migrate to genital ridge but fail to proliferate normally between 11.5 and 14.5 dpc
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• higher levels of activated caspase-3, p53, and Bax in extracts of 13.5 dpc mutant genital ridges than in controls, suggesting p53-related apoptosis of mutant PGCs
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• significantly smaller testes at 6 wks of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• median survival of 118 day
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• increased levels of proliferation and DNA damage are seen in lung tissue affected by lymphoma
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• lymphomas are more aggressive and most commonly infiltrate the lungs, liver and spleen with less frequent infiltration of the colon and kidney
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• develop aggressive and widespread lymphomas involving the lung, liver, thymus, bone marrow and peripheral blood with a significantly reduced latency compared to mice null for Trp53 alone
• about 86% of mice develop lymphomas
• seldom localized to the thymus
• most commonly infiltrate the lungs, liver and spleen with less frequent infiltration of the colon and kidney
• lymphoma cells often completely deplete the lungs, liver and spleen completely obscuring the normal anatomy of these tissues
• significant invasion of the bone marrow is seen
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• develop carcinomas in various organs with a significantly reduced latency compared to mice null for Trp53 alone
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• in pre-neoplastic splenocytes
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• accumulation of aneuploidy in splenocytes is seen as early as 2.5 months of age
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• increased proliferation in pre-neoplastic bone marrow cells
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• accumulation of aneuploidy in splenocytes is seen as early as 2.5 months of age
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• in pre-neoplastic splenocytes
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• in pre-neoplastic splenocytes
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• accumulation of aneuploidy in splenocytes is seen as early as 2.5 months of age
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| lymphoma | DOID:0060058 | J:174926 | ||
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• about 50% of mice develop carcinomas over a period of 460 days which is an increased incidence compared to mice heterozygous for the Trp53 mutation alone
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• die at E11.5
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• at E9.5 larger, lobed nuclei are seen in several organs, including the somites, heart, and brain
• after 10 days in culture MEFs have large lobed nuclei
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• 16 of 24 mitotic MEF cells had multipolar spindles and 8 were undergoing anaphase with lagging chromosomes
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• 16 of 24 mitotic MEF cells had multipolar spindles
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• extensive cell death is seen at E9.5
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• at E10.5
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• at E10.5
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• irregular somites are seen at E10.5
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• at E10.5
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• at E10.5
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• pups die prior to E12.5
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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 03/18/2025 MGI 6.24 |
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