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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Pnkptm1.1Pmc
targeted mutation 1.1, Peter J McKinnon
MGI:5795744
Summary 5 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Pnkptm1.1Pmc/Pnkptm1.1Pmc
Emx1tm1(cre)Krj/Emx1+
involves: 129S1/Sv * 129S2/SvPas * C57BL/6 MGI:5795755
cn2
Pnkptm1.1Pmc/Pnkptm1.1Pmc
Edil3Tg(Sox2-cre)1Amc/Edil3+
involves: 129S1/Sv * C57BL/6 * CBA MGI:5795747
cn3
Pnkptm1.1Pmc/Pnkptm1.1Pmc
Tg(CAG-cre/Esr1*)5Amc/0
involves: 129S1/Sv * C57BL/6 * CBA MGI:5795834
cn4
Atmtm2Pmc/Atmtm2Pmc
Pnkptm1.1Pmc/Pnkptm1.1Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * C57BL/6 * SJL MGI:5795758
cn5
Pnkptm1.1Pmc/Pnkptm1.1Pmc
Tg(Nes-cre)1Kln/0
involves: 129S1/Sv * C57BL/6 * SJL MGI:5795748


Genotype
MGI:5795755
cn1
Allelic
Composition
Pnkptm1.1Pmc/Pnkptm1.1Pmc
Emx1tm1(cre)Krj/Emx1+
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Emx1tm1(cre)Krj mutation (2 available); any Emx1 mutation (34 available)
Pnkptm1.1Pmc mutation (0 available); any Pnkp mutation (38 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• loss of all dorsal telencephalic progenitors via apoptosis
• proliferation in the cortex is reduced by E15.5 compared with E13.5

growth/size/body
• body size is reduced at P5

nervous system
• loss of all dorsal telencephalic progenitors via apoptosis
• brain size is reduced at P5
• almost complete absence of the cortex




Genotype
MGI:5795747
cn2
Allelic
Composition
Pnkptm1.1Pmc/Pnkptm1.1Pmc
Edil3Tg(Sox2-cre)1Amc/Edil3+
Genetic
Background
involves: 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Edil3Tg(Sox2-cre)1Amc mutation (5 available); any Edil3 mutation (43 available)
Pnkptm1.1Pmc mutation (0 available); any Pnkp mutation (38 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• early lethality, with no embryos recovered after E9




Genotype
MGI:5795834
cn3
Allelic
Composition
Pnkptm1.1Pmc/Pnkptm1.1Pmc
Tg(CAG-cre/Esr1*)5Amc/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pnkptm1.1Pmc mutation (0 available); any Pnkp mutation (38 available)
Tg(CAG-cre/Esr1*)5Amc mutation (10 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• mice treated with tamoxifen at P10 (3 doses every 2 days) exhibit apoptosis in the dentate gyrus at P20

growth/size/body
• mice treated with tamoxifen at P7 exhibit a decreased body size at P13
• mice treated with tamoxifen at P10 (3 doses every 2 days) exhibit a modest effect on brain size at P20

nervous system
• mice treated with tamoxifen at P10 (3 doses every 2 days) exhibit apoptosis in the dentate gyrus at P20
• mice treated with tamoxifen at P7 exhibit decreased brain size
• however, mice treated with tamoxifen at P21 (3 doses every 2 days) exhibit little overall effect on brain size or structure
• mice treated with tamoxifen at P7 exhibit a reduction in cortical size
• mice treated with tamoxifen at P21 (3 doses every 2 days) exhibit a decrease in oligodendrocyte numbers in the dentate gyrus but not in the cortex at P33
• mice treated with tamoxifen at P21 show a reduction of mature neurons in the dentate gyrus, the hippocampal CA3 region and the cerebellum
• myelin-producing oligodendrocytes from mice treated with tamoxifen at P21 show a reduction in myelination
• mice treated with tamoxifen at P10 (3 doses every 2 days) exhibit a loss of myelination in the dentate gyrus at P20
• mice treated with tamoxifen at P14 (3 doses every 2 days) exhibit a loss of myelination of oligodendrocytes at P30




Genotype
MGI:5795758
cn4
Allelic
Composition
Atmtm2Pmc/Atmtm2Pmc
Pnkptm1.1Pmc/Pnkptm1.1Pmc
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Atmtm2Pmc mutation (0 available); any Atm mutation (170 available)
Pnkptm1.1Pmc mutation (0 available); any Pnkp mutation (38 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• hemorrhage in the brain

cellular
• apoptosis in the developing cerebellum is similar to single conditional Pnkp mutants

nervous system
• hemorrhage in the brain
• apoptosis in the developing cerebellum is similar to single conditional Pnkp mutants
• reduction in cerebellar interneurons




Genotype
MGI:5795748
cn5
Allelic
Composition
Pnkptm1.1Pmc/Pnkptm1.1Pmc
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pnkptm1.1Pmc mutation (0 available); any Pnkp mutation (38 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice do not survive past 5 days of age

cellular
• mice show abundant cell death from E13 onwards throughout the developing nervous system
• apoptosis is seen in the developing cerebellum
• reduction in proliferation is seen in the developing nervous system
• primary astrocytes show a defect in the repair of DNA double strand breaks after bleomycin treatment
• primary cortical non-replicating astrocytes show a deficiency in the repair of DNA damage after treatment with ionizing radiation, hydrogen peroxide, or camptothecin

nervous system
• hemorrhage in the brain
• mice show abundant cell death from E13 onwards throughout the developing nervous system
• apoptosis is seen in the developing cerebellum
• reduction in cerebellar interneurons
• smaller cortex
• however, the layering of the cortex still occurs
• reduction in numbers of neurons in the cortex, particularly in later-born upper cortical layers

cardiovascular system
• hemorrhage in the brain

homeostasis/metabolism
• primary astrocytes show a defect in the repair of DNA double strand breaks after bleomycin treatment
• primary cortical non-replicating astrocytes show a deficiency in the repair of DNA damage after treatment with ionizing radiation, hydrogen peroxide, or camptothecin





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last database update
12/10/2024
MGI 6.24
The Jackson Laboratory