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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Ptentm1Mro
targeted mutation 1, Silvia Marino
MGI:2183284
Summary 16 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Braftm1Mmcm/Braf+
Ptentm1Mro/Ptentm1Mro
Tg(Tyr-cre/ERT2)1Lru/0
B6.Cg-Braftm1Mmcm Tg(Tyr-cre/ERT2)1Lru Ptentm1Mro MGI:5447169
cn2
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
involves: 129 * 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * FVB/N MGI:5563247
cn3
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Rb1tm2Brn/Rb1tm2Brn
involves: 129 * 129S4/SvJaeSor * C57BL/6 * FVB MGI:5563246
cn4
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Slc1a3tm1(cre/ERT2)Mgoe/Slc1a3+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJaeSor MGI:5790976
cn5
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJaeSor MGI:5790977
cn6
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * FVB MGI:5563238
cn7
Ptentm1Mro/Ptentm1Mro
Tg(KRT14-cre)8Brn/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * DBA/2J * FVB/N MGI:3842835
cn8
Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+
Ptentm1Mro/Pten+
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * FVB/N MGI:5427498
cn9
Ptentm1Mro/Pten+
Tg(KLK3-cre)D4Trp/0
involves: 129P2/OlaHsd * FVB MGI:3761927
cn10
Ptentm1Mro/Ptentm1Mro
Tg(KLK3-cre)D4Trp/0
involves: 129P2/OlaHsd * FVB MGI:3761928
cn11
Ptentm1Mro/Ptentm1Mro
Sdhbtm1.1Ics/Sdhbtm1.2Ics
Tg(KLK3-cre)D4Trp/0
involves: 129S2/SvPas * BALB/c * C57BL/6 * FVB MGI:5812678
cn12
Ptentm1Mro/Ptentm1Mro
Sdhbtm1.1Ics/Sdhb+
Tg(KLK3-cre)D4Trp/0
involves: 129S2/SvPas * FVB MGI:5812676
cn13
Ptentm1Mro/Pten+
Sdhbtm1.1Ics/Sdhb+
Tg(KLK3-cre)D4Trp/0
involves: 129S2/SvPas * FVB MGI:5812679
cn14
Ptentm1Mro/Pten+
Tg(Pbsn-cre)4Prb/0
involves: C57BL/6 * DBA/2 MGI:5427499
cn15
Ptentm1Mro/Ptentm1Mro
Tg(Pcp2-cre)756Mro/0
involves: FVB/N MGI:3805877
cn16
Ptentm1Mro/Ptentm1Mro
Tg(En2-cre)22Alj/0
Not Specified MGI:3805876


Genotype
MGI:5447169
cn1
Allelic
Composition
Braftm1Mmcm/Braf+
Ptentm1Mro/Ptentm1Mro
Tg(Tyr-cre/ERT2)1Lru/0
Genetic
Background
B6.Cg-Braftm1Mmcm Tg(Tyr-cre/ERT2)1Lru Ptentm1Mro
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Mmcm mutation (3 available); any Braf mutation (58 available)
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Tg(Tyr-cre/ERT2)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• tamoxifen-treated mice must be euthanized between 40 and 70 days due to tumor load or ulceration
• in tamoxifen treated mice

neoplasm
• tamoxifen-treated mice develop multiple heavily pigmented papules with an average latency of 18 days
• tamoxifen-treated mice exhibit metastasis in draining lymph nodes as early as 4 weeks after tumor induction
• however, no visceral metastasis is observed
• however, treatment with PLX4720 decreases tumor outgrowth
• in the absences of tamoxifen, most mice develop spontaneous melanomas due to leaky cre expression

integument
• in tamoxifen-treated mice
• tamoxifen-treated mice develop multiple heavily pigmented papules with an average latency of 18 days
• tamoxifen-treated mice exhibit metastasis in draining lymph nodes as early as 4 weeks after tumor induction
• however, no visceral metastasis is observed
• however, treatment with PLX4720 decreases tumor outgrowth
• in the absences of tamoxifen, most mice develop spontaneous melanomas due to leaky cre expression




Genotype
MGI:5563247
cn2
Allelic
Composition
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Rb1tm2Brn/Rb1tm2Brn
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129 * 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (8 available); any Gt(ROSA)26Sor mutation (942 available)
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (106 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle predominantly develop poorly differentiated, well-circumscribed neoplasms with similarity to supratentorial primitive neuroectodermal tumors (sPNET)
• expression profiles of tumors resemble human atypical teratoid/rhabdoid tumor

nervous system
• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle predominantly develop poorly differentiated, well-circumscribed neoplasms with similarity to supratentorial primitive neuroectodermal tumors (sPNET)
• expression profiles of tumors resemble human atypical teratoid/rhabdoid tumor




Genotype
MGI:5563246
cn3
Allelic
Composition
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Rb1tm2Brn/Rb1tm2Brn
Genetic
Background
involves: 129 * 129S4/SvJaeSor * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (8 available); any Gt(ROSA)26Sor mutation (942 available)
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (106 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle do not develop tumors after up to 440 days




Genotype
MGI:5790976
cn4
Allelic
Composition
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Slc1a3tm1(cre/ERT2)Mgoe/Slc1a3+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJaeSor
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (8 available); any Gt(ROSA)26Sor mutation (942 available)
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Slc1a3tm1(cre/ERT2)Mgoe mutation (0 available); any Slc1a3 mutation (66 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 3 of 16 mice injected with endoxifen develop glial tumors with lesions of different sizes and varying extents of infiltration
• small neoplastic lesions in endoxifen-induced mice arise from beneath the SVZ and extend into the striatum and dorsally into the corpus callosum
• larger tumors of endoxifen-induced mice show expansion into and a diffuse infiltration of the entire caudate nucleus
• some tumors contain areas of necrosis and occasional microvascular proliferations similar to those in malignant gliomas
• endoxifen-induced tumors show glial morphology with features typical of astrocytomas and oligodendrogliomas
• endoxifen-induced tumors show glial morphology with features typical of astrocytomas and oligodendrogliomas

nervous system
• 3 of 16 mice injected with endoxifen develop glial tumors with lesions of different sizes and varying extents of infiltration
• small neoplastic lesions in endoxifen-induced mice arise from beneath the SVZ and extend into the striatum and dorsally into the corpus callosum
• larger tumors of endoxifen-induced mice show expansion into and a diffuse infiltration of the entire caudate nucleus
• some tumors contain areas of necrosis and occasional microvascular proliferations similar to those in malignant gliomas
• endoxifen-induced tumors show glial morphology with features typical of astrocytomas and oligodendrogliomas
• endoxifen-induced tumors show glial morphology with features typical of astrocytomas and oligodendrogliomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
high grade glioma DOID:3070 OMIM:PS137800
J:229481




Genotype
MGI:5790977
cn5
Allelic
Composition
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (8 available); any Gt(ROSA)26Sor mutation (942 available)
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice injected with an adenovirus expressing cre recombinase (Ad-Cre) into the left ventricle exhibit a 33.3% incidence of glioma
• in left ventricle Ad-cre injected mice
• in left ventricle Ad-cre injected mice

nervous system
• mice injected with an adenovirus expressing cre recombinase (Ad-Cre) into the left ventricle exhibit a 33.3% incidence of glioma
• in left ventricle Ad-cre injected mice
• in left ventricle Ad-cre injected mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
high grade glioma DOID:3070 OMIM:PS137800
J:229481




Genotype
MGI:5563238
cn6
Allelic
Composition
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sortm1Sor
Ptentm1Mro/Ptentm1Mro
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (8 available); any Gt(ROSA)26Sor mutation (942 available)
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle develop a spectrum of gliomas, including anaplastic astrocytomas, oligodendrogliomas, and most commonly, anaplastic oligoastrocytomas
• however, adeno-cre injected mice do not develop glioblastoma with palisading necrosis or microvascular proliferation
• tumors in adeno-cre injected mice resemble The Cancer Genome Atlas (TCGA) classical glioblastomas, Phillips proneural and TACG neural gliomas
• mice injected with an adeno-cre into the lateral ventricle develop anaplastic oligoastrocytoma
• oligoastrocytomas do not resemble any human gliobastoma subtypes
• mice injected with an adeno-cre into the lateral ventricle develop oligodendrogliomas

nervous system
• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle develop a spectrum of gliomas, including anaplastic astrocytomas, oligodendrogliomas, and most commonly, anaplastic oligoastrocytomas
• however, adeno-cre injected mice do not develop glioblastoma with palisading necrosis or microvascular proliferation
• tumors in adeno-cre injected mice resemble The Cancer Genome Atlas (TCGA) classical glioblastomas, Phillips proneural and TACG neural gliomas
• mice injected with an adeno-cre into the lateral ventricle develop anaplastic oligoastrocytoma
• oligoastrocytomas do not resemble any human gliobastoma subtypes
• mice injected with an adeno-cre into the lateral ventricle develop oligodendrogliomas




Genotype
MGI:3842835
cn7
Allelic
Composition
Ptentm1Mro/Ptentm1Mro
Tg(KRT14-cre)8Brn/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * DBA/2J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Tg(KRT14-cre)8Brn mutation (4 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (232 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die by 20 weeks of age of unknown cause

neoplasm
• all mice develop malignant carcinomas in the oral cavity or lips by 18 weeks of age
• tumors are similar to those that develop in Trp53tm1Brn/Trp53tm1Brn Tg(KRT14-cre)8Brn Tg(KRT5-Akt1*)Jmpa mice

behavior/neurological
• mice display a progressive weakening




Genotype
MGI:5427498
cn8
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+
Ptentm1Mro/Pten+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki mutation (0 available); any Gt(ROSA)26Sor mutation (942 available)
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Prostate cancer progression in Tg(Pbsn-cre)4Prb/0 Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+, Tg(Pbsn-cre)4Prb/0 Ptentm1Mro/Pten+, and Tg(Pbsn-cre)4Prb/0 Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+ Ptentm1Mro/Pten+ mice

neoplasm
• 55% penetrance at 1 year
• multifocal, predominantly localized in the dorsolateral lobe that are locally invasive and highly vascularized

renal/urinary system

endocrine/exocrine glands
• 55% penetrance at 1 year
• multifocal, predominantly localized in the dorsolateral lobe that are locally invasive and highly vascularized

reproductive system
• 55% penetrance at 1 year
• multifocal, predominantly localized in the dorsolateral lobe that are locally invasive and highly vascularized




Genotype
MGI:3761927
cn9
Allelic
Composition
Ptentm1Mro/Pten+
Tg(KLK3-cre)D4Trp/0
Genetic
Background
involves: 129P2/OlaHsd * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Tg(KLK3-cre)D4Trp mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• at 4-5 months, epithelial cell lining of prostate tubules is disorganized, with tufting and/or cribriform growth patterns, unlike the regularly-layered columnar epithelial lining in controls
• epithelial cells are generally enlarged with some foci showing dysplasia characterized by cells with dense cytoplasm enlarged, somewhat vesicular nuclei with conspicuous nuclei
• at 7-9 months, distention of glands continues, with dysplasia becoming more diffuse
• prostate lobes are obviously enlarged compared with control prostates; at 4-5 months, average weight is increased 2-fold and at 7-9 months increase is 3-fold
• at 14 months with prostate cancer, weight has rapidly increased
• at 4-5 months of age, most glands of the different lobes show hyperplasia with accumulation of luminal cells, with distension of individual preexisting glands
• at 7-9 months hyperplasia continues to progress
• progressive tumor development is observed in mice at 4-5 months along with focal prostatic intraepithelial neoplasia (PIN) lesions, 7-9 months with more widespread PIN and focal microinvasion and at 10-14 months with invasive tumors
• in 14-month old mice, tumors are all shown to be epithelial in origin, classified as adenocarcinoma of poor, low or moderate grade differentiation

endocrine/exocrine glands
• at 4-5 months, epithelial cell lining of prostate tubules is disorganized, with tufting and/or cribriform growth patterns, unlike the regularly-layered columnar epithelial lining in controls
• epithelial cells are generally enlarged with some foci showing dysplasia characterized by cells with dense cytoplasm enlarged, somewhat vesicular nuclei with conspicuous nuclei
• at 7-9 months, distention of glands continues, with dysplasia becoming more diffuse
• prostate lobes are obviously enlarged compared with control prostates; at 4-5 months, average weight is increased 2-fold and at 7-9 months increase is 3-fold
• at 14 months with prostate cancer, weight has rapidly increased
• at 4-5 months of age, most glands of the different lobes show hyperplasia with accumulation of luminal cells, with distension of individual preexisting glands
• at 7-9 months hyperplasia continues to progress
• progressive tumor development is observed in mice at 4-5 months along with focal prostatic intraepithelial neoplasia (PIN) lesions, 7-9 months with more widespread PIN and focal microinvasion and at 10-14 months with invasive tumors
• in 14-month old mice, tumors are all shown to be epithelial in origin, classified as adenocarcinoma of poor, low or moderate grade differentiation

neoplasm
• progressive tumor development is observed in mice at 4-5 months along with focal prostatic intraepithelial neoplasia (PIN) lesions, 7-9 months with more widespread PIN and focal microinvasion and at 10-14 months with invasive tumors
• in 14-month old mice, tumors are all shown to be epithelial in origin, classified as adenocarcinoma of poor, low or moderate grade differentiation




Genotype
MGI:3761928
cn10
Allelic
Composition
Ptentm1Mro/Ptentm1Mro
Tg(KLK3-cre)D4Trp/0
Genetic
Background
involves: 129P2/OlaHsd * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Tg(KLK3-cre)D4Trp mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• mutants show a 2-fold higher number of proliferating (BrdU-positive) cells at 4-5, 7-9, and 10-14 months

endocrine/exocrine glands
• mutants show a 2-fold higher number of proliferating (BrdU-positive) cells at 4-5, 7-9, and 10-14 months




Genotype
MGI:5812678
cn11
Allelic
Composition
Ptentm1Mro/Ptentm1Mro
Sdhbtm1.1Ics/Sdhbtm1.2Ics
Tg(KLK3-cre)D4Trp/0
Genetic
Background
involves: 129S2/SvPas * BALB/c * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Sdhbtm1.1Ics mutation (0 available); any Sdhb mutation (27 available)
Sdhbtm1.2Ics mutation (0 available); any Sdhb mutation (27 available)
Tg(KLK3-cre)D4Trp mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 42% incidence of pheochromocytoma
• tumors do not show accumulation of succinate

neoplasm
• 42% incidence of pheochromocytoma
• tumors do not show accumulation of succinate




Genotype
MGI:5812676
cn12
Allelic
Composition
Ptentm1Mro/Ptentm1Mro
Sdhbtm1.1Ics/Sdhb+
Tg(KLK3-cre)D4Trp/0
Genetic
Background
involves: 129S2/SvPas * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Sdhbtm1.1Ics mutation (0 available); any Sdhb mutation (27 available)
Tg(KLK3-cre)D4Trp mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 89% of mice show pheochromocytoma at 12.9 months of age
• tumors do not show accumulation of succinate

neoplasm
• 89% of mice show pheochromocytoma at 12.9 months of age
• tumors do not show accumulation of succinate

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pheochromocytoma DOID:0050771 OMIM:171300
J:236514




Genotype
MGI:5812679
cn13
Allelic
Composition
Ptentm1Mro/Pten+
Sdhbtm1.1Ics/Sdhb+
Tg(KLK3-cre)D4Trp/0
Genetic
Background
involves: 129S2/SvPas * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Sdhbtm1.1Ics mutation (0 available); any Sdhb mutation (27 available)
Tg(KLK3-cre)D4Trp mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 64% of mice develop pheochromocytoma

neoplasm
• 64% of mice develop pheochromocytoma




Genotype
MGI:5427499
cn14
Allelic
Composition
Ptentm1Mro/Pten+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Prostate cancer progression in Tg(Pbsn-cre)4Prb/0 Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+, Tg(Pbsn-cre)4Prb/0 Ptentm1Mro/Pten+, and Tg(Pbsn-cre)4Prb/0 Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+ Ptentm1Mro/Pten+ mice

neoplasm

reproductive system

endocrine/exocrine glands




Genotype
MGI:3805877
cn15
Allelic
Composition
Ptentm1Mro/Ptentm1Mro
Tg(Pcp2-cre)756Mro/0
Genetic
Background
involves: FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Tg(Pcp2-cre)756Mro mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• mice exhibit subtle irregularities in the Purkinje cell lining compared to in wild-type mice
• increased in size compared to in wild-type mice
• at 17 and 20 weeks
• dendrites and descending axons are thickened compared to in wild-type mice




Genotype
MGI:3805876
cn16
Allelic
Composition
Ptentm1Mro/Ptentm1Mro
Tg(En2-cre)22Alj/0
Genetic
Background
Not Specified
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Mro mutation (1 available); any Pten mutation (81 available)
Tg(En2-cre)22Alj mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• migration of Purkinje cells is impaired with the majority of cells clustering above the fourth ventricle without recognizable orientation
• Golgi, stellate, basket, Bergmann glial and oligodendrocyte cells fail to migrate properly and are randomly distributed throughout the cerebellum
• at P1 and P9, cerebellar cell proliferation is increased and cell death is decreased compared to in wild-type mice
• at E15.5, mice exhibit increased precursor cell size resulting in an increase in cerebellar anlage size
• at E15.5, cerebellar cell proliferation is increased and cell death is decreased compared to in wild-type mice
• several Purkinje cells migrate towards the cerebellar surface and intermingle with granule cells
• unlike in wild-type mice, mature granule cells are found within the molecular layer due to disrupted migration
• the cerebellar vermis is enlarged after 3 weeks

behavior/neurological
• after 3 weeks mice exhibit ataxia that worsens until 8 weeks of age
• after 3 weeks
• after 3 weeks

neoplasm
N
• despite the loss of Pten in several human tumors including glioblastoma, mice do not exhibit any neoplastic transformation

cellular
• migration of Purkinje cells is impaired with the majority of cells clustering above the fourth ventricle without recognizable orientation
• Golgi, stellate, basket, Bergmann glial and oligodendrocyte cells fail to migrate properly and are randomly distributed throughout the cerebellum





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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory