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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Bmi1tm1Brn
targeted mutation 1, Anton Berns
MGI:1857632
Summary 14 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Bmi1tm1Brn/Bmi1tm1Brn either: (involves: 129P2/OlaHsd) or (involves: 129P2/OlaHsd * FVB) MGI:2658682
hm2
Bmi1tm1Brn/Bmi1tm1Brn involves: 129P2/OlaHsd MGI:2674270
hm3
Bmi1tm1Brn/Bmi1tm1Brn involves: 129P2/OlaHsd * C57BL/6J * FVB/N MGI:6850619
ht4
Bmi1tm1Brn/Bmi1+ involves: 129P2/OlaHsd MGI:2674271
cn5
Bmi1tm1Brn/Bmi1tm1Brn
Apctm2Cip/Apc+
Cdkn2atm1Cjs/Cdkn2atm1Cjs
Tg(Vil1-cre)20Syr/0
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * DBA/2 MGI:5532576
cn6
Bmi1tm1Brn/Bmi1tm1Brn
Apctm2Cip/Apc+
Tg(Vil1-cre)20Syr/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:5532574
cx7
Bmi1tm1Brn/Bmi1tm1Brn
Rnf2tm1Mvl/Rnf2+
involves: 129/Ola * FVB MGI:3852545
cx8
Pcgf2tm1Hko/Pcgf2tm1Hko
Bmi1tm1Brn/Bmi1+
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:3577617
cx9
Pcgf2tm1Hko/Pcgf2+
Bmi1tm1Brn/Bmi1tm1Brn
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:3577618
cx10
Pcgf2tm1Hko/Pcgf2tm1Hko
Bmi1tm1Brn/Bmi1tm1Brn
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6 MGI:3577619
cx11
Bmi1tm1Brn/Bmi1tm1Brn
E2f6tm1Lees/E2f6+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:3790813
cx12
Bmi1tm1Brn/Bmi1tm1Brn
E2f6tm1Lees/E2f6tm1Lees
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:3790810
cx13
Bmi1tm1Brn/Bmi1+
E2f6tm1Lees/E2f6tm1Lees
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:3790811
cx14
Bmi1tm1Brn/Bmi1+
E2f6tm1Lees/E2f6+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:3790812


Genotype
MGI:2658682
hm1
Allelic
Composition
Bmi1tm1Brn/Bmi1tm1Brn
Genetic
Background
either: (involves: 129P2/OlaHsd) or (involves: 129P2/OlaHsd * FVB)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• animals die between 3-20 weeks of age from repeated illnesses
• about 50% of animals die between postnatal days 1-3; pups are selectively cannibalized by their mothers

behavior/neurological
• ataxic gait is first noticeable at 2-4 weeks of age and becomes progressively more severe with age
• walking is uncoordinated and mice fall over onto their side frequently

growth/size/body
• mice that survive the first few days after birth are smaller

hematopoietic system
• proliferative response of adult, but not newborn, splenocytes to LPS or ConA stimulation is reduced 8-10-fold compared to wild-type
• number of thymocytes is decreased to less than 1% of wild-type
• involuted thymus
• hematopoieisis is severely reduced
• hematopoietic cell counts are reduced to about 30% of wild-type levels
• absolute number of immature B cells (B220+HSA+ and B220+BPl+) is significantly reduced
• the immature CD4-CD8- thymocyte population is increased from 4% of total cells in wild-type to 90% of total cells in mutants, although in absolute numbers, this population size is decreased to 12% of wild-type, indicating the presence of mainly immature thymocytes
• moribund mice exhibit anemia
• in colony assays, bone marrow cells do not respond to IL-7 or to LPS
• in colony assays, the number of myeloid colonies induced by L-cell-conditioned medium containing M-CSF, is reduced 4-10 fold
• decrease in cell numbers and replacement of large areas of hematopoiesis by adipoctyes in the bone marrow
• number of mature B cells (B220+sIg+) is significantly reduced
• hypoplasia of the red pulp
• hypoplasia of the white pulp
• serum IgM levels are reduced to 70% of wild-type levels

immune system
• proliferative response of adult, but not newborn, splenocytes to LPS or ConA stimulation is reduced 8-10-fold compared to wild-type
• number of thymocytes is decreased to less than 1% of wild-type
• involuted thymus
• absolute number of immature B cells (B220+HSA+ and B220+BPl+) is significantly reduced
• the immature CD4-CD8- thymocyte population is increased from 4% of total cells in wild-type to 90% of total cells in mutants, although in absolute numbers, this population size is decreased to 12% of wild-type, indicating the presence of mainly immature thymocytes
• number of mature B cells (B220+sIg+) is significantly reduced
• hypoplasia of the red pulp
• hypoplasia of the white pulp
• serum IgM levels are reduced to 70% of wild-type levels
• moribound mice exhibit pneumonia

skeleton
• broadening and splitting of the neural arch of the atlas or the axis
• skeletal transformations affecting vertebrae; incomplete penetrance, although each mutant has at least one transformation and 87% have multiple transformations
• transformation of T7 to T8, resulting in the presence of six vertebrosternal ribs instead of seven in controls
• transformation of T13 to the first lumbar vertebra (L1), as evidenced by the absence or degeneration of the ribs normally associated with T13
• transformation of the seventh cervical vertebra (C7) to the first thoracic vertebra (T1), as evidenced by the presence of ribs at C7, which fuse on the ventral side with the ribs associated with T1
• transformation of L6 to the first sacral vertebra (S1), as evidenced by the association of the ilial bones with L6 instead of S1 as in controls

nervous system
• dark shrunken and degenerating neurons are seen in some mutants
• reduced thickness of cerebellar layers, neuron loss
• shrunken Purkinje cells
• major white matter tracts, such as the corpus callosum, show extensive gliosis

respiratory system
• moribound mice exhibit pneumonia

cellular
• proliferative response of adult, but not newborn, splenocytes to LPS or ConA stimulation is reduced 8-10-fold compared to wild-type

endocrine/exocrine glands
• number of thymocytes is decreased to less than 1% of wild-type
• involuted thymus




Genotype
MGI:2674270
hm2
Allelic
Composition
Bmi1tm1Brn/Bmi1tm1Brn
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• lethality is seen between 3 and 20 weeks of age
• about half as many mice as expected are present at weaning however no reduction in numbers is detected at E18.5

growth/size/body

skeleton
• small extra bone present above C1 in 29% of homozygous mice
• transformation of T7 to T8 and T13 to L1 are seen in 71% and 57% of homozygous mice, respectively
• transformation of C1 to C2 and C7 to T1 are seen in 57% and 29% of homozygous mice, respectively
• partial transformation of C7 to T1 is seen in 43% of homozygous mice
• transformation of L6 to S1 is seen in 86% of homozygous mice

hematopoietic system
• severe
• shift in the distribution of myeloid to B lymphoid cells resulting in an increased percentage of myeloid cells
• within the B cell population, loss of immature B cells is greater than the loss of mature B cells
• decreased number of hematopoietic cells in the thymus, bone marrow and spleen

reproductive system
• over 50% of sperm exhibit severe malformations at 7 weeks of age
• mitochondrial contents are significantly reduced in the sperm mitochondrial sheath
• numerous sperm head defects are observed, including irregular, sharp and big heads
• several genes required for sperm shaping are significantly downregulated
• sperm nucleus is detached from the acrosome
• sperm exhibit nuclear condensation defects
• germ cell counts are reduced in the seminiferous tubule epithelium at 7 weeks of age
• CASA analysis of sperm counts in caudal epididymis revealed severe oligospermia at 7 weeks of age
• male germ cell proliferation is severely reduced, as determined by Ki67 immunostaining in testicular sections
• male germ cell apoptosis is markedly increased, as determined by a TUNEL assay in testicular sections
• seminiferous tubule epithelium is highly disorganized at 7 weeks of age
• seminiferous tubule diameters are reduced at 7 weeks of age
• Leydig cell population (3betaHSD positive cells) is significantly reduced at 7 weeks of age
• testis size is significantly smaller than that in wild-type controls at 7 weeks of age
• testis weight is significantly reduced at 7 weeks of age
• both p16 and p53 immunopositive cells in testis are significantly increased and the protein expression levels of p16, p19, p53 and p21 are markedly up-regulated in testis extracts from 7-week-old male mice
• reactive oxygen species (ROS) and (H2O2) levels are significantly increased whereas total antioxidant capacity and the expression levels of antioxidant enzyme genes (Gpx1, Gsr, Cat, Txnrd1) are decreased
• numbers of 8-OHdG positive cells and gammaH2AX positive cells are dramatically increased in testicular sections, indicating increased DNA damage
• testosterone production is reduced and both mRNA and protein levels of Hsd3b1 (3betaHSD) and Hsd17b1 (17betaHSD) are significantly downregulated in testis extracts from 7-week-old male mice
• round immature germ cell like cells are found in epididymal sections at 7 weeks of age
• male mice mated with adult wild-type females of proven fertility for 1 month are unable to produce offspring, indicating complete male sterility

cellular
• over 50% of sperm exhibit severe malformations at 7 weeks of age
• mitochondrial contents are significantly reduced in the sperm mitochondrial sheath
• numerous sperm head defects are observed, including irregular, sharp and big heads
• several genes required for sperm shaping are significantly downregulated
• sperm nucleus is detached from the acrosome
• sperm exhibit nuclear condensation defects
• germ cell counts are reduced in the seminiferous tubule epithelium at 7 weeks of age
• CASA analysis of sperm counts in caudal epididymis revealed severe oligospermia at 7 weeks of age
• impaired ability of serum-starved MEFs to re-enter the cell cycle
• defect in asynchronous proliferation in MEFs
• in MEFs (J:134271)
• in mouse embryonic fibroblasts by passage 6 (J:198334)
• male germ cell proliferation is severely reduced, as determined by Ki67 immunostaining in testicular sections
• male germ cell apoptosis is markedly increased, as determined by a TUNEL assay in testicular sections
• reactive oxygen species (ROS) and hydrogen peroxide (H2O2) levels are significantly increased whereas total antioxidant capacity and the expression levels of antioxidant enzyme genes (Gpx1, Gsr, Cat, Txnrd1) are decreased in testis extracts from 7-week-old male mice

behavior/neurological
• seen in mice that survive to 2 months of age

nervous system
• all three layers are affected

immune system

endocrine/exocrine glands
• seminiferous tubule epithelium is highly disorganized at 7 weeks of age
• seminiferous tubule diameters are reduced at 7 weeks of age
• Leydig cell population (3betaHSD positive cells) is significantly reduced at 7 weeks of age
• testis size is significantly smaller than that in wild-type controls at 7 weeks of age
• testis weight is significantly reduced at 7 weeks of age
• both p16 and p53 immunopositive cells in testis are significantly increased and the protein expression levels of p16, p19, p53 and p21 are markedly up-regulated in testis extracts from 7-week-old male mice
• reactive oxygen species (ROS) and (H2O2) levels are significantly increased whereas total antioxidant capacity and the expression levels of antioxidant enzyme genes (Gpx1, Gsr, Cat, Txnrd1) are decreased
• numbers of 8-OHdG positive cells and gammaH2AX positive cells are dramatically increased in testicular sections, indicating increased DNA damage
• testosterone production is reduced and both mRNA and protein levels of Hsd3b1 (3betaHSD) and Hsd17b1 (17betaHSD) are significantly downregulated in testis extracts from 7-week-old male mice

homeostasis/metabolism
• serum testosterone levels are significantly reduced at 7 weeks of age
• both mRNA and protein levels of Hsd3b1 (3betaHSD) and Hsd17b1 (17betaHSD) are significantly downregulated in testis extracts from 7-week-old male mice
• expression levels of antioxidant enzyme genes including Gpx1, Gsr, Cat, Txnrd1 are decreased in testis extracts




Genotype
MGI:6850619
hm3
Allelic
Composition
Bmi1tm1Brn/Bmi1tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• number of retrieved oocytes per mouse is significantly lower than that for wild-type females
• administration of antioxidant N-acetylcysteine (NAC) in the drinking water from 3 to 7 weeks of age increases the number of retrieved oocytes significantly but does not restore oocyte number to wild-type levels
• the number of mature follicles per ovary is markedly reduced at 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age results in a marked increase in mature ovarian follicle number
• the number of primary follicles per ovary is markedly reduced at 1, 4, and 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age has no significant effect on primary ovarian follicle number
• the number of primordial follicles per ovary is markedly reduced at 1, 4, and 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age has no significant effect on primordial ovarian follicle number
• the number of secondary follicles per ovary is markedly reduced at 4 and 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age results in a marked increase in secondary ovarian follicle number
• the number of atretic ovarian follicles is markedly increased at 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age results in a marked decrease in atretic follicle number
• ovary size is significantly smaller at 7 weeks of age
• administration of antioxidant N-acetylcysteine (NAC) in the drinking water from 3 to 7 weeks of age results in a marked increase in ovary size
• ovarian weight and ovarian weight/body weight ratio are significantly decreased at 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age results in a marked increase in ovarian weight and ovarian weight/body weight ratio
• protein levels of p16, p19 and p53 are markedly increased whereas anti-apoptotic BCL-2 protein levels are decreased in ovarian extracts from 7-week-old female mice
• numbers of 8-OHdG+ cells and gammaH2AX+ cells are dramatically increased in ovarian sections at 7 weeks of age, indicating increased DNA damage
• % of BrdU+ cells is significantly reduced at 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age results in markedly reduced numbers of 8-OHdG+ cells and gammaH2AX+ cells while % of BrdU+ cells is increased
• % of Caspase-3+ granulosa cells is significantly increased at 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age results in markedly reduced % of Caspase-3+ cells
• % of PCNA+ granulosa cells is significantly reduced at 7 weeks of age
• vaginal opening time is markedly delayed
• following induction of superovulation with PMSG and hCG, significantly fewer oocytes are retrieved from the ampulla portion of 3-week old females relative to similarly treated wild-type females
• % of time spent in diestrus per 5 days is significantly increased
• % of time spent in estrus per 5 days is significantly reduced
• % of time spent in metestrus per 5 days is significantly increased
• % of time spent in proestrus per 5 days is significantly reduced
• female mice mated with adult wild-type males of known fertility for 1 month fail to produce offspring, indicating complete female sterility

cellular
• number of retrieved oocytes per mouse is significantly lower than that for wild-type females
• administration of antioxidant N-acetylcysteine (NAC) in the drinking water from 3 to 7 weeks of age increases the number of retrieved oocytes significantly but does not restore oocyte number to wild-type levels
• TEM images of granulosa cells and oocytes showed that the mitochondrial outer membrane is indistinct and defective
• some mitochondrial crest blurring or even swelling is observed in the ovaries
• the number of mitochondria is significantly reduced in the ovaries at 7 weeks of age
• % of Caspase-3+ granulosa cells is significantly increased at 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age results in markedly reduced % of Caspase-3+ cells
• % of PCNA+ granulosa cells is significantly reduced at 7 weeks of age
• flow cytometry analysis showed increased reactive oxygen species (ROS) levels in the ovaries at 7 weeks of age
• mRNA expression levels of antioxidant enzyme genes (Sod1, Sod2, Gpx1, Gsr, Cat, and Txnrd1) and the protein levels of SOD1 and SOD2 are significantly decreased in ovarian extracts from 7-week-old female mice
• antioxidant NAC administration from 3 to 7 weeks of age results in markedly decreased ROS levels while protein levels of SOD1 and SOD2 are significantly increased

homeostasis/metabolism
• mRNA expression levels of antioxidant enzyme genes (Sod1, Sod2, Gpx1, Gsr, Cat, and Txnrd1) and the protein levels of SOD1 and SOD2 are significantly decreased in ovarian extracts from 7-week-old female mice
• both mRNA and protein levels of Sod1 (superoxide dismutase 1) and Sod2 (superoxide dismutase 2) are significantly decreased in ovarian extracts from 7-week-old female mice

embryo
• in vitro, oocytes derived from mice treated with IVF fail to develop into 2-cell stage embryos
• surprisingly, antioxidant NAC supplementation rescues the ability of oocytes to develop into early embryos in vitro (including 2-cells, 4-cells, and blastocysts) to nearly wild-type levels

endocrine/exocrine glands
• the number of mature follicles per ovary is markedly reduced at 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age results in a marked increase in mature ovarian follicle number
• the number of primary follicles per ovary is markedly reduced at 1, 4, and 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age has no significant effect on primary ovarian follicle number
• the number of primordial follicles per ovary is markedly reduced at 1, 4, and 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age has no significant effect on primordial ovarian follicle number
• the number of secondary follicles per ovary is markedly reduced at 4 and 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age results in a marked increase in secondary ovarian follicle number
• the number of atretic ovarian follicles is markedly increased at 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age results in a marked decrease in atretic follicle number
• ovary size is significantly smaller at 7 weeks of age
• administration of antioxidant N-acetylcysteine (NAC) in the drinking water from 3 to 7 weeks of age results in a marked increase in ovary size
• ovarian weight and ovarian weight/body weight ratio are significantly decreased at 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age results in a marked increase in ovarian weight and ovarian weight/body weight ratio
• protein levels of p16, p19 and p53 are markedly increased whereas anti-apoptotic BCL-2 protein levels are decreased in ovarian extracts from 7-week-old female mice
• numbers of 8-OHdG+ cells and gammaH2AX+ cells are dramatically increased in ovarian sections at 7 weeks of age, indicating increased DNA damage
• % of BrdU+ cells is significantly reduced at 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age results in markedly reduced numbers of 8-OHdG+ cells and gammaH2AX+ cells while % of BrdU+ cells is increased
• % of Caspase-3+ granulosa cells is significantly increased at 7 weeks of age
• antioxidant NAC administration from 3 to 7 weeks of age results in markedly reduced % of Caspase-3+ cells
• % of PCNA+ granulosa cells is significantly reduced at 7 weeks of age




Genotype
MGI:2674271
ht4
Allelic
Composition
Bmi1tm1Brn/Bmi1+
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• transformation of T13 to L1 is seen in 13% of heterozygous mice
• partial or complete transformation of C7 to T1 is seen in 31% and 19% of heterozygous mice, respectively
• transformation of L6 to S1 is seen in 50% of heterozygous mice




Genotype
MGI:5532576
cn5
Allelic
Composition
Bmi1tm1Brn/Bmi1tm1Brn
Apctm2Cip/Apc+
Cdkn2atm1Cjs/Cdkn2atm1Cjs
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2Cip mutation (0 available); any Apc mutation (154 available)
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (33 available)
Cdkn2atm1Cjs mutation (6 available); any Cdkn2a mutation (62 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• found in some animals by 90 days of age

behavior/neurological
• hunching appears in some animals at 90 days of age

neoplasm
• increased size and number of small intestine adenomas

digestive/alimentary system
• increased size and number of small intestine adenomas




Genotype
MGI:5532574
cn6
Allelic
Composition
Bmi1tm1Brn/Bmi1tm1Brn
Apctm2Cip/Apc+
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2Cip mutation (0 available); any Apc mutation (154 available)
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (33 available)
Tg(Vil1-cre)20Syr mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tumors in small intestine are almost absent at 120 days of age
• fewer and smaller tumors at 90 days of age as well
• decrease in numbers of tumors between 90 and 120 days
• no increase in tumor size between 90 and 120 days
• also reduced at 120 days
• adenomas are one tenth the size of those found in controls at 120 days of age
• increased cell proliferation in adenomas at 90 days
• increased apoptosis in smaller adenomas but not larger ones at 90 days
• apoptosis is also increased in non tumor tissue

cellular
• increased apoptosis in smaller adenomas but not larger ones at 90 days
• apoptosis is also increased in non tumor tissue

digestive/alimentary system
• tumors in small intestine are almost absent at 120 days of age
• fewer and smaller tumors at 90 days of age as well
• decrease in numbers of tumors between 90 and 120 days
• no increase in tumor size between 90 and 120 days
• also reduced at 120 days
• adenomas are one tenth the size of those found in controls at 120 days of age
• increased cell proliferation in adenomas at 90 days
• increased apoptosis in smaller adenomas but not larger ones at 90 days
• apoptosis is also increased in non tumor tissue




Genotype
MGI:3852545
cx7
Allelic
Composition
Bmi1tm1Brn/Bmi1tm1Brn
Rnf2tm1Mvl/Rnf2+
Genetic
Background
involves: 129/Ola * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (33 available)
Rnf2tm1Mvl mutation (0 available); any Rnf2 mutation (36 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants die at 4-5 weeks of age, earlier than single homozygous Bmi1 mutants

growth/size/body
• delay in postnatal development at P10, from which point onward, growth ceases almost entirely

behavior/neurological
• severe lack of coordination
• mutants exhibit a more abnormal gait than single homozygous Bmi1 mutants impaired coordination [MP:0001405

nervous system
• arborization of Purkinje cells in the molecular layer is different, with thicker and less branched dendrites
• reduction in cellularity and size of the granular layer of the cerebellum
• reduction in cellularity and size of the molecular layer of the cerebellum

skeleton
• mutants exhibit axial skeleton abnormalities in the cervical, thoracic, lumbar and sacral regions




Genotype
MGI:3577617
cx8
Allelic
Composition
Pcgf2tm1Hko/Pcgf2tm1Hko
Bmi1tm1Brn/Bmi1+
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (33 available)
Pcgf2tm1Hko mutation (2 available); any Pcgf2 mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial

skeleton
• acromion is poorly formed
• holes are seen in the blade of the scapula
• ectopic ossification centers in sternum
• rudimentary ribs attached to C6
• atlas resembles the third cervical vertebra
• atlas resembles the third cervical vertebra

digestive/alimentary system

growth/size/body




Genotype
MGI:3577618
cx9
Allelic
Composition
Pcgf2tm1Hko/Pcgf2+
Bmi1tm1Brn/Bmi1tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (33 available)
Pcgf2tm1Hko mutation (2 available); any Pcgf2 mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
craniofacial

skeleton
• acromion is poorly formed
• holes are seen in the blade of the scapula
• ectopic ossification centers in sternum
• rudimentary ribs attached to C6
• atlas resembles the third cervical vertebra
• atlas resembles the third cervical vertebra

digestive/alimentary system

growth/size/body




Genotype
MGI:3577619
cx10
Allelic
Composition
Pcgf2tm1Hko/Pcgf2tm1Hko
Bmi1tm1Brn/Bmi1tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S1/Sv * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (33 available)
Pcgf2tm1Hko mutation (2 available); any Pcgf2 mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

cardiovascular system
• dorsal aorta is expanded in the caudal region

embryo
• first branchial arches were poorly developed
• second branchial arches were poorly developed
• development was normal at E8.5 but mice were severely growth retarded at E9.5
• somatic mesoderm was appropriately segmented but irregularly aligned
• neural tube is small
• cell to cell adhesion is impaired in the neural tube
• fusion with hindgut endoderm seen
• reduced
• bifurcated
• 18 as opposed to the normal 24 somites at E9.5
• distal tip of the tail bud is shrunken

nervous system
• apoptosis is seen in the neural tube
• neural tube is small
• cell to cell adhesion is impaired in the neural tube
• hindbrain is underdeveloped

skeleton
• atlas resembles the third cervical vertebra
• atlas resembles the third cervical vertebra

craniofacial
• first branchial arches were poorly developed
• second branchial arches were poorly developed

limbs/digits/tail
• distal tip of the tail bud is shrunken

vision/eye
• optic eminence was obscure

cellular
• apoptosis is seen in the neural tube




Genotype
MGI:3790813
cx11
Allelic
Composition
Bmi1tm1Brn/Bmi1tm1Brn
E2f6tm1Lees/E2f6+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (33 available)
E2f6tm1Lees mutation (0 available); any E2f6 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• small extra bone present above C1 in 62% of compound mutant mice
• transformation of T7 to T8 and T13 to L1 are seen in 77% and 85% of compound mutant mice, respectively
• transformation of C1 to C2, C5 to C6, and C7 to T1 are seen in 85%, 23%, and 31% of compound mutant mice, respectively
• partial transformation of C7 to T1 is seen in 77% of compound mutant mice
• transformation of L6 to S1 is seen in 92% of compound mutant mice




Genotype
MGI:3790810
cx12
Allelic
Composition
Bmi1tm1Brn/Bmi1tm1Brn
E2f6tm1Lees/E2f6tm1Lees
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (33 available)
E2f6tm1Lees mutation (0 available); any E2f6 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• lethality is seen between 3 and 20 weeks of age
• only 38% of the expected number of mice are present at weaning
• only 46% of the expected number of embryos are present at E18.5

growth/size/body

skeleton
• small extra bone present above C1 in 38% of double homozygous mice
• transformation of T7 to T8 and T13 to L1 are seen in 62% and 100% of double homozygous mice, respectively
• transformation of C1 to C2, C5 to C6, and C7 to T1 are seen in 92%, 23%, and 8% of double homozygous mice, respectively
• partial transformation of C7 to T1 is seen in 85% of double homozygous mice
• transformation of L6 to S1 is seen in 100% of double homozygous mice

hematopoietic system
• severe
• shift in the distribution of myeloid to B lymphoid cells resulting in an increased percentage of myeloid cells
• within the B cell population, loss of immature B cells is greater than the loss of mature B cells
• decreased number of hematopoietic cells in the thymus, bone marrow and spleen

cellular
• impaired ability of serum-starved MEFs to re-enter the cell cycle
• defect in asynchronous proliferation in MEFs

behavior/neurological
• similar to that seen in mice homozygous for Bmi1tm1Brn alone at 2 months of age

nervous system
• all three layers are affected
• hypoplasia is similar to that in mice homozygous for Bmi1tm1Brn alone

immune system




Genotype
MGI:3790811
cx13
Allelic
Composition
Bmi1tm1Brn/Bmi1+
E2f6tm1Lees/E2f6tm1Lees
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (33 available)
E2f6tm1Lees mutation (0 available); any E2f6 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• transformation of T13 to L1 is seen in 77% of compound mutant mice
• partial or complete transformation of C7 to T1 is seen in 27% and 4% of compound mutant mice, respectively
• transformation of L6 to S1 is seen in 92% of compound mutant mice




Genotype
MGI:3790812
cx14
Allelic
Composition
Bmi1tm1Brn/Bmi1+
E2f6tm1Lees/E2f6+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bmi1tm1Brn mutation (2 available); any Bmi1 mutation (33 available)
E2f6tm1Lees mutation (0 available); any E2f6 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
skeleton
• transformation of T7 to T8 and T13 to L1 are seen in 4% and 50% of double heterozygous mice, respectively
• partial or complete transformation of C7 to T1 is seen in 42% and 8% of double heterozygous mice, respectively
• transformation of C5 to C6 is seen in 4% of double heterozygous mice
• transformation of L6 to S1 is seen in 73% of double heterozygous mice





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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
03/19/2024
MGI 6.23
The Jackson Laboratory