About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Atrtm2Bal
targeted mutation 2, David Baltimore
MGI:2656567
Summary 8 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Atrtm2Bal/Atrtm2Bal
Cdkn2atm2Brn/Cdkn2atm2Brn
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL MGI:5316228
cn2
Atrtm1Bal/Atrtm2Bal
Tg(UBC-cre/ERT2)1Ejb/0
involves: 129S/SvEv * 129S2/SvPas * C57BL/6 MGI:3717476
cn3
Atrtm1Bal/Atrtm2Bal
Tg(Syn1-cre)671Jxm/0
involves: 129S/SvEv * 129S2/SvPas * C57BL/6 * CBA MGI:3717477
cn4
Atrtm2Bal/Atrtm2Bal
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S2/SvPas * C57BL/6 * CBA MGI:5316225
cn5
Atrtm2Bal/Atrtm2Bal
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:5316221
cn6
Atrtm2Bal/Atrtm2Bal
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:5316227
cn7
Atmtm2Pmc/Atmtm2Pmc
Atrtm2Bal/Atrtm2Bal
Tg(Nes-cre)1Kln/0
involves: 129S2/SvPas * C57BL/6 * SJL MGI:5316230
cn8
Atrtm2Bal/Atrtm2Bal
Emx1tm1(cre)Krj/Emx1+
involves: 129S2/SvPas * C57BL/6J MGI:5316224


Genotype
MGI:5316228
cn1
Allelic
Composition
Atrtm2Bal/Atrtm2Bal
Cdkn2atm2Brn/Cdkn2atm2Brn
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atrtm2Bal mutation (0 available); any Atr mutation (10 available)
Cdkn2atm2Brn mutation (2 available); any Cdkn2a mutation (26 available)
Tg(Nes-cre)1Kln mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• similar neuropathology to mutant mice wild-type for Cdkn2a (J:181920)
• similar neuropathology to mutant mice wild-type for Cdkn2a (J:181920)




Genotype
MGI:3717476
cn2
Allelic
Composition
Atrtm1Bal/Atrtm2Bal
Tg(UBC-cre/ERT2)1Ejb/0
Genetic
Background
involves: 129S/SvEv * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atrtm1Bal mutation (0 available); any Atr mutation (10 available)
Atrtm2Bal mutation (0 available); any Atr mutation (10 available)
Tg(UBC-cre/ERT2)1Ejb mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• 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) (J:123200)
• 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) (J:123200)

pigmentation
• 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 (J:123200)
• 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 (J:123200)

skeleton
• between 3 and 12 months after tamoxifen treatment, mice show significant kyphosis relative to control mice (J:123200)
• between 3 and 12 months after tamoxifen treatment, mice show significant kyphosis relative to control mice (J:123200)
• 1 year after tamoxifen treatment, mice show an 18% decrease in cortical bone cross-sectional area as determined by micro-CT (J:123200)
• 1 year after tamoxifen treatment, mice show an 18% decrease in cortical bone cross-sectional area as determined by micro-CT (J:123200)
• 1 year after tamoxifen treatment, mice show a 46-76% reduction in trabecular bone volume as determined by micro-CT (J:123200)
• 1 year after tamoxifen treatment, mice show a 46-76% reduction in trabecular bone volume as determined by micro-CT (J:123200)
• after tamoxifen treatment, mice begin to develop osteoporosis (J:123200)
• after tamoxifen treatment, mice begin to develop osteoporosis (J:123200)

endocrine/exocrine glands
• 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 (J:123200)
• 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 (J:123200)
• hair follicles often display sebaceous gland cell hyperplasia (J:123200)
• hair follicles often display sebaceous gland cell hyperplasia (J:123200)
• mice display premature thymic involution (~1 year) after tamoxifen treatment (J:123200)
• mice display premature thymic involution (~1 year) after tamoxifen treatment (J:123200)

hematopoietic system
• 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 (J:123200)
• 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 (J:123200)
• mice display premature thymic involution (~1 year) after tamoxifen treatment (J:123200)
• mice display premature thymic involution (~1 year) after tamoxifen treatment (J:123200)

immune system
• 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 (J:123200)
• 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 (J:123200)
• mice display premature thymic involution (~1 year) after tamoxifen treatment (J:123200)
• mice display premature thymic involution (~1 year) after tamoxifen treatment (J:123200)
• leukocyte infiltration of the kidneys is observed in all tamoxifen-treated mice at 1 year post-treatment (J:123200)
• leukocyte infiltration of the kidneys is observed in all tamoxifen-treated mice at 1 year post-treatment (J:123200)

liver/biliary system
• a significant increase in senescence-associated betagalactosidase-positive cells is observed in the liver 1 year after tamoxifen treatment (J:123200)
• a significant increase in senescence-associated betagalactosidase-positive cells is observed in the liver 1 year after tamoxifen treatment (J:123200)

renal/urinary system
• leukocyte infiltration of the kidneys is observed in all tamoxifen-treated mice at 1 year post-treatment (J:123200)
• leukocyte infiltration of the kidneys is observed in all tamoxifen-treated mice at 1 year post-treatment (J:123200)
• by 1 year after tamoxifen treatment, kidneys display atrophy (J:123200)
• by 1 year after tamoxifen treatment, kidneys display atrophy (J:123200)
• glomerular degeneration in all kidneys of tamoxifen-treated mice at 1 year after treatment, but not in controls (J:123200)
• glomerular degeneration in all kidneys of tamoxifen-treated mice at 1 year after treatment, but not in controls (J:123200)
• tubular degeneration in all kidneys of tamoxifen-treated mice at 1 year after treatment (J:123200)
• tubular degeneration in all kidneys of tamoxifen-treated mice at 1 year after treatment (J:123200)
• fibrotic tissue accumulates in kidneys of tamoxifen-treated mice with age (J:123200)
• fibrotic tissue accumulates in kidneys of tamoxifen-treated mice with age (J:123200)

digestive/alimentary system
• 1 week after tamoxifen treatment, ~80% of villus epithelium is lost, but recovers fully by 1 months after treatment (J:123200)
• 1 week after tamoxifen treatment, ~80% of villus epithelium is lost, but recovers fully by 1 months after treatment (J:123200)

cardiovascular system
• compared to control mice, fibrotic tissue accumulates in hearts of tamoxifen-treated mice with age (J:123200)
• compared to control mice, fibrotic tissue accumulates in hearts of tamoxifen-treated mice with age (J:123200)

adipose tissue
• layer is reduced up to 70% in thickness 3-6 months after tamoxifen treatment (J:123200)
• layer is reduced up to 70% in thickness 3-6 months after tamoxifen treatment (J:123200)

cellular
• temporary loss of proliferating cells after tamoxifen treatment is observed in intestine, skin, kidney and liver (J:123200)
• temporary loss of proliferating cells after tamoxifen treatment is observed in intestine, skin, kidney and liver (J:123200)

integument
• layer is reduced up to 70% in thickness 3-6 months after tamoxifen treatment (J:123200)
• layer is reduced up to 70% in thickness 3-6 months after tamoxifen treatment (J:123200)
• hair follicles often display sebaceous gland cell hyperplasia (J:123200)
• hair follicles often display sebaceous gland cell hyperplasia (J:123200)
• 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 (J:123200)
• 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 (J:123200)
• after a third round of depilation, hair regrowth does not occur or regrows predominantly gray (J:123200)
• after a third round of depilation, hair regrowth does not occur or regrows predominantly gray (J:123200)
• 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 (J:123200)
• single topical doses of 4-hydroxytamoxifen to skin causes alopecia and gray hair regrowth (J:123200)
• 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 (J:123200)
• single topical doses of 4-hydroxytamoxifen to skin causes alopecia and gray hair regrowth (J:123200)
• remaining follicles in mice >6 months display gray shafts (J:123200)
• after depilation in tamoxifen-treated mice, hair shaft generation is delayed and compromised in abundance and quality (J:123200)
• remaining follicles in mice >6 months display gray shafts (J:123200)
• after depilation in tamoxifen-treated mice, hair shaft generation is delayed and compromised in abundance and quality (J:123200)
• remaining hair follicles often show abnormal architecture with degeneration of dermal and epidermal structures (J:123200)
• remaining hair follicles often show abnormal architecture with degeneration of dermal and epidermal structures (J:123200)
• significantly delayed after tamoxifen treatment (J:123200)
• development is delayed in anagen after tamoxifen treatment (J:123200)
• significantly delayed after tamoxifen treatment (J:123200)
• development is delayed in anagen after tamoxifen treatment (J:123200)
• loss of hair follicles is observed 3-6 months after tamoxifen treatment (J:123200)
• loss of hair follicles is observed 3-6 months after tamoxifen treatment (J:123200)
• 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 (J:123200)
• after a second round of depilation in telogen phase, hair regrowth is more sparse, with increased representation of gray hair shafts (J:123200)
• 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 (J:123200)
• after a second round of depilation in telogen phase, hair regrowth is more sparse, with increased representation of gray hair shafts (J:123200)
• after a second round of depilation in telogen phase, hair regrowth is more sparse, with increased representation of gray hair shafts (J:123200)
• after a second round of depilation in telogen phase, hair regrowth is more sparse, with increased representation of gray hair shafts (J:123200)
• mice develop thickened epidermis 3-6 months after tamoxifen treatment (J:123200)
• mice develop thickened epidermis 3-6 months after tamoxifen treatment (J:123200)




Genotype
MGI:3717477
cn3
Allelic
Composition
Atrtm1Bal/Atrtm2Bal
Tg(Syn1-cre)671Jxm/0
Genetic
Background
involves: 129S/SvEv * 129S2/SvPas * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atrtm1Bal mutation (0 available); any Atr mutation (10 available)
Atrtm2Bal mutation (0 available); any Atr mutation (10 available)
Tg(Syn1-cre)671Jxm mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
N
• tamoxifen-treated mice do not show any significant differences from controls in circadian activity, strength, motor coordination, anxiety-like behavior, learning or memory (J:123200)
• tamoxifen-treated mice do not show any significant differences from controls in circadian activity, strength, motor coordination, anxiety-like behavior, learning or memory (J:123200)




Genotype
MGI:5316225
cn4
Allelic
Composition
Atrtm2Bal/Atrtm2Bal
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atrtm2Bal mutation (0 available); any Atr mutation (10 available)
Tg(CAG-cre/Esr1*)5Amc mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• decrease in proliferation in cultured neurospheres after 4OHT treatment (J:181920)
• decrease in proliferation in cultured neurospheres after 4OHT treatment (J:181920)

nervous system
• decrease in proliferation in cultured neurospheres after 4OHT treatment (J:181920)
• decrease in proliferation in cultured neurospheres after 4OHT treatment (J:181920)




Genotype
MGI:5316221
cn5
Allelic
Composition
Atrtm2Bal/Atrtm2Bal
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atrtm2Bal mutation (0 available); any Atr mutation (10 available)
Tg(Nes-cre)1Kln mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• die by P7 (J:181920)
• die by P7 (J:181920)

nervous system
• elevated apoptosis is detected in the external granule cell layer at E16.5 (J:181920)
• high levels of DNA damage and elevated apoptosis in the ganglionic eminence at E15.5 (J:181920)
• elevated apoptosis is detected in the external granule cell layer at E16.5 (J:181920)
• high levels of DNA damage and elevated apoptosis in the ganglionic eminence at E15.5 (J:181920)
• striking decrease in proliferation at E16.5 in the rhombic lip (J:181920)
• decrease in the size and growth of neurospheres indicating a defect in proliferation (J:181920)
• striking decrease in proliferation at E16.5 in the rhombic lip (J:181920)
• decrease in the size and growth of neurospheres indicating a defect in proliferation (J:181920)
• striking decrease in proliferation at E16.5 in the cerebellar external granule cell layer (J:181920)
• striking decrease in proliferation at E16.5 in the cerebellar external granule cell layer (J:181920)
• marked defects in cerebellar development (J:181920)
• marked defects in cerebellar development (J:181920)
• striking decrease in proliferation at E16.5 in the rhombic lip (J:181920)
• striking decrease in proliferation at E16.5 in the rhombic lip (J:181920)
• decreased cellularity (J:181920)
• decreased cellularity (J:181920)
• decreased cellularity, especially in the upper layers (J:181920)
• decreased cellularity, especially in the upper layers (J:181920)
• depleted (J:181920)
• depleted (J:181920)
• mislocalization of Purkinje cells (J:181920)
• mislocalization of Purkinje cells (J:181920)
• defects in foliation and mislocalization of Purkinje cells (J:181920)
• defects in foliation and mislocalization of Purkinje cells (J:181920)
• high levels of DNA damage and elevated apoptosis in the ganglionic eminence at E15.5 (J:181920)
• high levels of DNA damage and elevated apoptosis in the ganglionic eminence at E15.5 (J:181920)

growth/size/body

cellular
• elevated apoptosis is detected in the external granule cell layer at E16.5 (J:181920)
• high levels of DNA damage and elevated apoptosis in the ganglionic eminence at E15.5 (J:181920)
• elevated apoptosis is detected in the external granule cell layer at E16.5 (J:181920)
• high levels of DNA damage and elevated apoptosis in the ganglionic eminence at E15.5 (J:181920)
• striking decrease in proliferation at E16.5 in the rhombic lip (J:181920)
• decrease in the size and growth of neurospheres indicating a defect in proliferation (J:181920)
• striking decrease in proliferation at E16.5 in the rhombic lip (J:181920)
• decrease in the size and growth of neurospheres indicating a defect in proliferation (J:181920)
• striking decrease in proliferation at E16.5 in the cerebellar external granule cell layer (J:181920)
• striking decrease in proliferation at E16.5 in the cerebellar external granule cell layer (J:181920)




Genotype
MGI:5316227
cn6
Allelic
Composition
Atrtm2Bal/Atrtm2Bal
Trp53tm1Tyj/Trp53tm1Tyj
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atrtm2Bal mutation (0 available); any Atr mutation (10 available)
Tg(Nes-cre)1Kln mutation (3 available)
Trp53tm1Tyj mutation (9 available); any Trp53 mutation (142 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• attenuated apoptosis in the external granule layer and ganglionic eminence compared to mutant mice wild-type for Trp53 (J:181920)
• partial rescue of apoptosis in the forebrain compared to mutant mice wild-type for Trp53 (J:181920)
• attenuated apoptosis in the external granule layer and ganglionic eminence compared to mutant mice wild-type for Trp53 (J:181920)
• partial rescue of apoptosis in the forebrain compared to mutant mice wild-type for Trp53 (J:181920)
• substantial enhancement of neurosphere size and growth compared to mutant mice wild-type for Trp53 (J:181920)
• however, after 7 days in culture expansion stops and cells fail to survive (J:181920)
• substantial enhancement of neurosphere size and growth compared to mutant mice wild-type for Trp53 (J:181920)
• however, after 7 days in culture expansion stops and cells fail to survive (J:181920)
• similar neuropathology to mutant mice wild-type for Trp53 (J:181920)
• similar neuropathology to mutant mice wild-type for Trp53 (J:181920)

cellular
• attenuated apoptosis in the external granule layer and ganglionic eminence compared to mutant mice wild-type for Trp53 (J:181920)
• partial rescue of apoptosis in the forebrain compared to mutant mice wild-type for Trp53 (J:181920)
• attenuated apoptosis in the external granule layer and ganglionic eminence compared to mutant mice wild-type for Trp53 (J:181920)
• partial rescue of apoptosis in the forebrain compared to mutant mice wild-type for Trp53 (J:181920)
• substantial enhancement of neurosphere size and growth compared to mutant mice wild-type for Trp53 (J:181920)
• however, after 7 days in culture expansion stops and cells fail to survive (J:181920)
• substantial enhancement of neurosphere size and growth compared to mutant mice wild-type for Trp53 (J:181920)
• however, after 7 days in culture expansion stops and cells fail to survive (J:181920)




Genotype
MGI:5316230
cn7
Allelic
Composition
Atmtm2Pmc/Atmtm2Pmc
Atrtm2Bal/Atrtm2Bal
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atmtm2Pmc mutation (0 available); any Atm mutation (30 available)
Atrtm2Bal mutation (0 available); any Atr mutation (10 available)
Tg(Nes-cre)1Kln mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• decrease in apoptosis in the external granule layer and ganglionic eminence compared to mutant mice wild-type for Atm (J:181920)
• decrease in apoptosis in the external granule layer and ganglionic eminence compared to mutant mice wild-type for Atm (J:181920)
• similar neuropathology to mutant mice wild-type for Atm (J:181920)
• similar neuropathology to mutant mice wild-type for Atm (J:181920)

cellular
• decrease in apoptosis in the external granule layer and ganglionic eminence compared to mutant mice wild-type for Atm (J:181920)
• decrease in apoptosis in the external granule layer and ganglionic eminence compared to mutant mice wild-type for Atm (J:181920)
• resistance to radiation induced DNA damage-induced apoptosis in neural tissues (J:181920)
• resistance to radiation induced DNA damage-induced apoptosis in neural tissues (J:181920)




Genotype
MGI:5316224
cn8
Allelic
Composition
Atrtm2Bal/Atrtm2Bal
Emx1tm1(cre)Krj/Emx1+
Genetic
Background
involves: 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atrtm2Bal mutation (0 available); any Atr mutation (10 available)
Emx1tm1(cre)Krj mutation (2 available); any Emx1 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• decreased in size and cellularity (J:181920)
• decreased in size and cellularity (J:181920)
• reduced cellularity (J:181920)
• reduced cellularity (J:181920)
• moderate perturbation of cortical development (J:181920)
• reduced cellularity, particularly in layers IV-II (J:181920)
• moderate perturbation of cortical development (J:181920)
• reduced cellularity, particularly in layers IV-II (J:181920)
• decrease in layer demarcation, particularly in layers IV-II (J:181920)
• decrease in layer demarcation, particularly in layers IV-II (J:181920)





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Tumor Biology (MTB), Gene Ontology (GO), MouseCyc
Citing These Resources
Funding Information
Warranty Disclaimer & Copyright Notice
Send questions and comments to User Support.
last database update
02/02/2016
MGI 6.02
The Jackson Laboratory