Analysis Tools
nervous system
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• similar neuropathology to mutant mice wild-type for Cdkn2a
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Allele Symbol Allele Name Allele ID |
Atrtm2Bal targeted mutation 2, David Baltimore MGI:2656567 |
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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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• similar neuropathology to mutant mice wild-type for Cdkn2a
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 1 year after tamoxifen treatment, treated mice show a 20% decrease in body weigh compared to controls (21.3 g vs 26.6 g in controls)
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• when mice are treated with tamoxifen at 8-12 weeks of age, within 3-4 months pervasive graying of the coat is observed; no obvious phenotype is observed in controls
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• between 3 and 12 months after tamoxifen treatment, mice show significant kyphosis relative to control mice
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• 1 year after tamoxifen treatment, mice show an 18% decrease in cortical bone cross-sectional area as determined by micro-CT
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• 1 year after tamoxifen treatment, mice show a 46-76% reduction in trabecular bone volume as determined by micro-CT
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• after tamoxifen treatment, mice begin to develop osteoporosis
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• by 1-2 weeks after tamoxifen treatment, relative to controls, mice show marked suppression of thymocyte numbers which recover by 3-4 months after treatment; 6-7 months after treatment, numbers are significantly decreased again relative to controls
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• hair follicles often display sebaceous gland cell hyperplasia
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• mice display premature thymic involution (~1 year) after tamoxifen treatment
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• by 1-2 weeks after tamoxifen treatment, relative to controls, mice show marked suppression of thymocyte numbers which recover by 3-4 months after treatment; 6-7 months after treatment, numbers are significantly decreased again relative to controls
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• mice display premature thymic involution (~1 year) after tamoxifen treatment
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• by 1-2 weeks after tamoxifen treatment, relative to controls, mice show marked suppression of thymocyte numbers which recover by 3-4 months after treatment; 6-7 months after treatment, numbers are significantly decreased again relative to controls
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• mice display premature thymic involution (~1 year) after tamoxifen treatment
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• leukocyte infiltration of the kidneys is observed in all tamoxifen-treated mice at 1 year post-treatment
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• a significant increase in senescence-associated betagalactosidase-positive cells is observed in the liver 1 year after tamoxifen treatment
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• leukocyte infiltration of the kidneys is observed in all tamoxifen-treated mice at 1 year post-treatment
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• by 1 year after tamoxifen treatment, kidneys display atrophy
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• glomerular degeneration in all kidneys of tamoxifen-treated mice at 1 year after treatment, but not in controls
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• tubular degeneration in all kidneys of tamoxifen-treated mice at 1 year after treatment
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• fibrotic tissue accumulates in kidneys of tamoxifen-treated mice with age
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• 1 week after tamoxifen treatment, ~80% of villus epithelium is lost, but recovers fully by 1 months after treatment
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• compared to control mice, fibrotic tissue accumulates in hearts of tamoxifen-treated mice with age
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• layer is reduced up to 70% in thickness 3-6 months after tamoxifen treatment
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• temporary loss of proliferating cells after tamoxifen treatment is observed in intestine, skin, kidney and liver
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• layer is reduced up to 70% in thickness 3-6 months after tamoxifen treatment
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• hair follicles often display sebaceous gland cell hyperplasia
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• when mice are treated with tamoxifen at 8-12 weeks of age, within 3-4 months pervasive graying of the coat is observed; no obvious phenotype is observed in controls
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• after a third round of depilation, hair regrowth does not occur or regrows predominantly gray
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• when mice are treated with tamoxifen at 8-12 weeks of age, a progressive alopecia develops within 3-4 months, increasing in expressivity past 1 year of age
• single topical doses of 4-hydroxytamoxifen to skin causes alopecia and gray hair regrowth
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• remaining follicles in mice >6 months display gray shafts
• after depilation in tamoxifen-treated mice, hair shaft generation is delayed and compromised in abundance and quality
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• remaining hair follicles often show abnormal architecture with degeneration of dermal and epidermal structures
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• significantly delayed after tamoxifen treatment
• development is delayed in anagen after tamoxifen treatment
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• loss of hair follicles is observed 3-6 months after tamoxifen treatment
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• following depilation in tamoxifen-treated mice, anagen phase is accompanied by widespread degenerative follicles 4 days after depilation and delay in anagen progression 8 days after depilation
• after a second round of depilation in telogen phase, hair regrowth is more sparse, with increased representation of gray hair shafts
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• after a second round of depilation in telogen phase, hair regrowth is more sparse, with increased representation of gray hair shafts
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• mice develop thickened epidermis 3-6 months after tamoxifen treatment
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• tamoxifen-treated mice do not show any significant differences from controls in circadian activity, strength, motor coordination, anxiety-like behavior, learning or memory
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• decrease in proliferation in cultured neurospheres after 4OHT treatment
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• decrease in proliferation in cultured neurospheres after 4OHT treatment
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• die by P7
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• elevated apoptosis is detected in the external granule cell layer at E16.5
• high levels of DNA damage and elevated apoptosis in the ganglionic eminence at E15.5
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• striking decrease in proliferation at E16.5 in the rhombic lip
• decrease in the size and growth of neurospheres indicating a defect in proliferation
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• striking decrease in proliferation at E16.5 in the cerebellar external granule cell layer
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• marked defects in cerebellar development
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• striking decrease in proliferation at E16.5 in the rhombic lip
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• decreased cellularity
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• decreased cellularity, especially in the upper layers
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• depleted
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• mislocalization of Purkinje cells
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• defects in foliation and mislocalization of Purkinje cells
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• high levels of DNA damage and elevated apoptosis in the ganglionic eminence at E15.5
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• elevated apoptosis is detected in the external granule cell layer at E16.5
• high levels of DNA damage and elevated apoptosis in the ganglionic eminence at E15.5
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• striking decrease in proliferation at E16.5 in the rhombic lip
• decrease in the size and growth of neurospheres indicating a defect in proliferation
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• striking decrease in proliferation at E16.5 in the cerebellar external granule cell layer
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• attenuated apoptosis in the external granule layer and ganglionic eminence compared to mutant mice wild-type for Trp53
• partial rescue of apoptosis in the forebrain compared to mutant mice wild-type for Trp53
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• substantial enhancement of neurosphere size and growth compared to mutant mice wild-type for Trp53
• however, after 7 days in culture expansion stops and cells fail to survive
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• similar neuropathology to mutant mice wild-type for Trp53
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• attenuated apoptosis in the external granule layer and ganglionic eminence compared to mutant mice wild-type for Trp53
• partial rescue of apoptosis in the forebrain compared to mutant mice wild-type for Trp53
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• substantial enhancement of neurosphere size and growth compared to mutant mice wild-type for Trp53
• however, after 7 days in culture expansion stops and cells fail to survive
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• decrease in apoptosis in the external granule layer and ganglionic eminence compared to mutant mice wild-type for Atm
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• similar neuropathology to mutant mice wild-type for Atm
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• resistance to radiation induced DNA damage-induced apoptosis in neural tissues
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• decrease in apoptosis in the external granule layer and ganglionic eminence compared to mutant mice wild-type for Atm
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• decreased in size and cellularity
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• reduced cellularity
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• moderate perturbation of cortical development
• reduced cellularity, particularly in layers IV-II
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• decrease in layer demarcation, particularly in layers IV-II
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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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