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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Bcl2tm1Dlo
targeted mutation 1, Dennis Y Loh
MGI:2156165
Summary 11 genotypes


Genotype
MGI:2176748
hm1
Allelic
Composition
Bcl2tm1Dlo/Bcl2tm1Dlo
Genetic
Background
B6.129P2-Bcl2tm1Dlo
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl2tm1Dlo mutation (0 available); any Bcl2 mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

The Bcl2l11tm3.1Boui mutation ameliorates the degenerative disorders of Bcl2tm1Dlo/Bcl2tm1Dlo mice

mortality/aging
• Background Sensitivity: this phenotype is more severe on an inbred C57BL/6 background than on a mixed 129 C57BL/6 background (J:73316)
• all homozygotes die from polycystic kidney disease between 3 and 8 weeks of age (J:73316)
• all homozygotes die from polycystic kidney disease between 2 and 4 weeks of age (J:104487)
• die by 50 days of age from the renal failure induced by polycystic kidney disease (PKD) (J:153846)

growth/size/body
• all homozygotes have short ears
• Background Sensitivity: this phenotype is more severe on an inbred C57BL/6 background than on a mixed 129 C57BL/6 background (J:73316)
• some cysts are present at P0 (J:73316)
• all homozygotes die from polycystic kidney disease between 3 and 8 weeks of age (J:73316)
• die by 50 days of age from the renal failure induced by polycystic kidney disease (PKD) (J:153846)
• Background Sensitivity: this phenotype is more severe on an inbred C57BL/6 background than on a mixed 129 C57BL/6 background (J:73316)
• all homozygotes become runted (J:73316)
• become runted (J:153846)
• decreased body weight at day 40

hearing/vestibular/ear
• all homozygotes have short ears

immune system
• presence of many apoptotic cell clusters
• irradiated mice reconstituted with mutant fetal liver cells have a 4- to 5- fold reduction in lymphocytes and myeloid cells compared to controls
• 5-10 mg vs. 60-100 mg in wild type
• atrophied spleen
• very few lymphoid follicles
• survival of mature resting T and B cells in the absence of cytokines is impaired compared to wild-type cells (J:73316)
• less than 1% of B cells are alive after 4 days of culturing without cytokines compared to over 10% of controls
• less than 1% of T cells are alive after 4 days of culturing without cytokines compared to over 10% of controls
• culturing with IL-7 fails to rescue T cells from apoptosis

renal/urinary system
• Background Sensitivity: this phenotype is more severe on an inbred C57BL/6 background than on a mixed 129 C57BL/6 background (J:73316)
• some cysts are present at P0 (J:73316)
• all homozygotes die from polycystic kidney disease between 3 and 8 weeks of age (J:73316)
• die by 50 days of age from the renal failure induced by polycystic kidney disease (PKD) (J:153846)
• at E15.5 metanephroi are smaller mostly as a result of reduced mesenchymal area of the cortex
• neonates have fewer nephrons and a narrower nephrogenic area
• at E15.5 the mesenchymal area of the cortex is reduced
• at E15.5 metanephroi are smaller mostly as a result of reduced mesenchymal area of the cortex
• neonates exhibit a narrower nephrogenic area
• neonates have fewer nephrons

craniofacial
• all homozygotes have short ears

hematopoietic system
• presence of many apoptotic cell clusters
• irradiated mice reconstituted with mutant fetal liver cells have a 4- to 5- fold reduction in lymphocytes and myeloid cells compared to controls
• 5-10 mg vs. 60-100 mg in wild type
• atrophied spleen
• very few lymphoid follicles
• survival of mature resting T and B cells in the absence of cytokines is impaired compared to wild-type cells (J:73316)
• less than 1% of B cells are alive after 4 days of culturing without cytokines compared to over 10% of controls
• less than 1% of T cells are alive after 4 days of culturing without cytokines compared to over 10% of controls
• culturing with IL-7 fails to rescue T cells from apoptosis

cellular
• less than 1% of B cells are alive after 4 days of culturing without cytokines compared to over 10% of controls
• less than 1% of T cells are alive after 4 days of culturing without cytokines compared to over 10% of controls
• culturing with IL-7 fails to rescue T cells from apoptosis
• presence of many apoptotic cell clusters




Genotype
MGI:2176707
hm2
Allelic
Composition
Bcl2tm1Dlo/Bcl2tm1Dlo
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl2tm1Dlo mutation (0 available); any Bcl2 mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

\AlleleSymbol (MGI:2156165|0)/Bcl2tm1Dlo with littermate control

mortality/aging
• about 50% die between 1 and 6 weeks after birth

pigmentation
• hair color turns gray postnatally between 4 and 5 weeks, however skin is normal

growth/size/body
• rounder nose
• kidneys exhibit a polycystic appearance
• body weight is 30-90% of controls

immune system
• number of lymphocytes in the peripheral blood, bone marrow, thymus, spleen, and lymph nodes decreases with age, while the number of segmented neutrophils and other hematopoietic lineages is normal
• more than 80% reduction of B220+/surface immunoglobulin-positive mature B cells in the bone marrow
• more than 80% reduction of B220+ surface immunoglobulin-negative pre-B cells in the bone marrow
• accelerated decrease over time in the percentage of CD4-CD8+ cells in the periphery

renal/urinary system
• at E13-E16, homozygotes show a 5-fold increase in nick end-labeled apoptotic cells per kidney area relative to wild-type controls (J:33776)
• at E13-E16, apoptotic cells and phagocytosed apoptotic bodies are often detected among uninduced mesenchymal cells and less frequently among induced tubular and peritubular cells (J:33776)
• at E13-E16, projections from intact mesenchymal cells are in contact with the cell membrane of apoptotic cells; in some cases, 2-3 apoptotic cells are seen together (J:33776)
• at E17-E19, homozygotes show a 5-fold increase in apoptotic cells per nephrogenic zone relative to wild-type and heterozygous controls (J:33776)
• increased kidney apoptosis throughout the tubular epithelium and the interstitium after P20 (J:111022)
• apoptosis is neither found in non-sclerotic glomeruli nor in stages prior to sclerosis (P20) (J:111022)
• apoptotic bodies first seen in severely injured or sclerotic glomeruli at P20
• kidneys have a nonsmooth surface, are pale, and exhibit interstitial hyperproliferation
• at P13, renal arteries and veins are abnormally located immediately beneath the kidney surface
• kidneys exhibit a polycystic appearance
• disarray of the cortex structure (J:73660)
• at P7-8, the renal cortex is thin, abnormally formed, and composed of only one nephron layer, unlike in control mice (J:111022)
• vacuolar degeneration of parietal epithelial cells after P20
• loss of urinary space at sites of glomerular synechiae
• starting at P12, podocytes show striking injuries, including cell body attenuation, pseudocyst formation, and accumulation of lysosomal elements
• vacuolar degeneration of podocytes after P20
• foot process effacement starting at P12
• binucleated podocytes are occasionally observed, indicating extreme cell hypertrophy
• at E17-E19, no centrifugal maturation of glomeruli is observed, unlike in control mice
• nuclear shrinkage of endothelial cells after P20
• increased matrix deposition starting at P12
• focal mesangiolysis starting at P12
• starting at P20, enlarged glomeruli develop segmental sclerosis rapidly progressing to global sclerosis
• by P56, almost all glomeruli are sclerotic
• at E17-E19, the nephrogenic zone contains only ~20% of the glomerular number found in control mice (J:33776)
• at P0-P2, glomeruli are rarely encountered in the deep cortex (J:33776)
• prior to P20, the number of glomeruli per unit volume cortex is ~20% of that in wild-type controls (J:111022)
• extensive tuft adhesions to Bowman's capsule after P20
• at E18, only a few, but large, glomeruli are observed in the deep cortex (J:33776)
• at P7-8, some glomeruli appear hypertrophied (J:111022)
• after P8, the volume of non-sclerotic glomeruli is 4x higher than that of wild-type controls (J:111022)
• by P56, non-sclerotic glomeruli are few in number and severely hypertrophied (J:111022)
• at P0-P2, the margin between the renal cortex and the medulla is indistinct, unlike in control mice
• at E17-E19, homozygotes display inactive nephrogenesis, probably as a result of fulminant apoptosis in the mesenchyme at E13-E16
• however, initial induction of nephrons at E13 is normal
• at E17, the nephrogenic zone is thin with immature tubuli scattered among the residual uninduced mesenchyme
• at E17-E19, a 5-fold increase in the number of apoptotic cells is noted in the nephrogenic zone
• at P0-P2, the nephrogenic zone is extremely thin and consists of uninduced mesenchymal cells
• dilated renal tubules with hypertrophic epithelium
• disarray of the medulla structure
• at P0-P2, homozygotes display smaller kidneys than wild-type or heterozygous control mice (J:33776)
• at P7-8, mutant kidneys are smaller than wild-type (J:111022)
• significantly reduced kidney weight from P7 to P56
• however, kidney growth rate is normal
• homozygotes display severe renal hypoplasia
• at E17-E19, homozygotes exhibit one-fifth of the nephron number found in control mice (J:33776)
• at P7-8, nephron number is dramatically reduced (J:111022)
• severe oligonephria is established at birth (J:111022)
• at P0-P2, several homozygotes display scattered dilatation in the lumen of renal tubules (J:33776)
• dilated renal tubules with hypertrophic epithelium (J:73660)
• after P8, hypertrophic tubules are dilated (J:111022)
• at E17-E19, proximal and distal tubuli are found in the deep layer with enlargement (J:33776)
• at P0-P2, renal tubuli are hypertrophic (J:33776)
• at P7-8, some tubules appear hypertrophied (J:111022)
• after birth, kidney structural damage rapidly progresses to glomerulosclerosis and cystic renal degeneration
• at E18, only rare convolution of ureteric buds is observed in the subcapsular area, unlike in control mice
• at P0-P2, ends of ureteric buds are occasionally observed in the subcapsular layer but are not convoluted
• at P0-P2, ureteric buds rarely extend to the subcapsular region, unlike in control mice
• neonatal UBs only extend as far as the deep layer of the kidney
• at P0-P2, ureteric buds are slender
• renal failure develops soon after birth

hearing/vestibular/ear

hematopoietic system
• number of lymphocytes in the peripheral blood, bone marrow, thymus, spleen, and lymph nodes decreases with age, while the number of segmented neutrophils and other hematopoietic lineages is normal
• more than 80% reduction of B220+/surface immunoglobulin-positive mature B cells in the bone marrow
• more than 80% reduction of B220+ surface immunoglobulin-negative pre-B cells in the bone marrow
• accelerated decrease over time in the percentage of CD4-CD8+ cells in the periphery

craniofacial
• rounder nose

integument
• hair color turns gray postnatally between 4 and 5 weeks, however skin is normal

cellular
• at E13-E16, homozygotes show a 5-fold increase in nick end-labeled apoptotic cells per kidney area relative to wild-type controls (J:33776)
• at E13-E16, apoptotic cells and phagocytosed apoptotic bodies are often detected among uninduced mesenchymal cells and less frequently among induced tubular and peritubular cells (J:33776)
• at E13-E16, projections from intact mesenchymal cells are in contact with the cell membrane of apoptotic cells; in some cases, 2-3 apoptotic cells are seen together (J:33776)
• at E17-E19, homozygotes show a 5-fold increase in apoptotic cells per nephrogenic zone relative to wild-type and heterozygous controls (J:33776)
• increased kidney apoptosis throughout the tubular epithelium and the interstitium after P20 (J:111022)
• apoptosis is neither found in non-sclerotic glomeruli nor in stages prior to sclerosis (P20) (J:111022)
• apoptotic bodies first seen in severely injured or sclerotic glomeruli at P20

cardiovascular system
• at P13, renal arteries and veins are abnormally located immediately beneath the kidney surface
• nuclear shrinkage of endothelial cells after P20

endocrine/exocrine glands

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
oligomeganephronia DOID:0111142 J:111022




Genotype
MGI:2176747
cx3
Allelic
Composition
Bcl2tm1Dlo/Bcl2tm1Dlo
Bcl2l11tm1.1Ast/Bcl2l11+
Genetic
Background
B6.129-Bcl2tm1Dlo Bcl2l11tm1.1Ast
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl2l11tm1.1Ast mutation (4 available); any Bcl2l11 mutation (32 available)
Bcl2tm1Dlo mutation (0 available); any Bcl2 mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice are healthy through at least 6 months of age

pigmentation
• coat color becomes gray at 5 to 7 weeks of age during completion of the second hair follicle cycle
• from the second follicle cycle on all newly grown hairs lack melanin and when an area is shaved the coat appears white suggesting the gray color is a result of unshed hairs from the first cycle
• by 5 to 7 weeks of age melanocytes are lost from the hair follicles
• absent from hair starting at the second hair follicle cycle
• coat colors become grey after two hair follicle cycles
• in areas where skin is shaved, hair comes back completely white

hearing/vestibular/ear
N
• ear length is normal

immune system
• survival of mature resting T and B cells in the absence of cytokines is improved compared to cells from mice homozygous for Bcl2tm1Dlo alone
• culturing with IL-7 only partially rescues T cells from apoptosis

renal/urinary system
N
• mice do not develop polycystic kidney disease

integument
• coat color becomes gray at 5 to 7 weeks of age during completion of the second hair follicle cycle
• from the second follicle cycle on all newly grown hairs lack melanin and when an area is shaved the coat appears white suggesting the gray color is a result of unshed hairs from the first cycle
• by 5 to 7 weeks of age melanocytes are lost from the hair follicles
• absent from hair starting at the second hair follicle cycle
• coat colors become grey after two hair follicle cycles
• in areas where skin is shaved, hair comes back completely white

cellular
• culturing with IL-7 only partially rescues T cells from apoptosis

hematopoietic system
• survival of mature resting T and B cells in the absence of cytokines is improved compared to cells from mice homozygous for Bcl2tm1Dlo alone
• culturing with IL-7 only partially rescues T cells from apoptosis




Genotype
MGI:2176749
cx4
Allelic
Composition
Bcl2tm1Dlo/Bcl2tm1Dlo
Bcl2l11tm1.1Ast/Bcl2l11tm1.1Ast
Genetic
Background
B6.129-Bcl2tm1Dlo Bcl2l11tm1.1Ast
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl2l11tm1.1Ast mutation (4 available); any Bcl2l11 mutation (32 available)
Bcl2tm1Dlo mutation (0 available); any Bcl2 mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice are healthy through at least 6 months of age

hearing/vestibular/ear
N
• ear length is normal

immune system
• irradiated mice reconstituted with mutant fetal liver cells have an increase in lymphocyte and myeloid cell numbers compared to controls
• survival of mature resting T and B cells in the absence of cytokines is improved compared to cells from mice homozygous for Bcl2tm1Dlo alone and cells from wild-type mice
• about 10-fold more B cells cultured without cytokines are alive after six days compared to controls
• culturing with IL-7 only partially rescues T cells from apoptosis over a 6 day period

renal/urinary system
N
• mice do not develop polycystic kidney disease

hematopoietic system
• irradiated mice reconstituted with mutant fetal liver cells have an increase in lymphocyte and myeloid cell numbers compared to controls
• survival of mature resting T and B cells in the absence of cytokines is improved compared to cells from mice homozygous for Bcl2tm1Dlo alone and cells from wild-type mice
• about 10-fold more B cells cultured without cytokines are alive after six days compared to controls
• culturing with IL-7 only partially rescues T cells from apoptosis over a 6 day period

integument
N
• coat color is normal

cellular
• about 10-fold more B cells cultured without cytokines are alive after six days compared to controls
• culturing with IL-7 only partially rescues T cells from apoptosis over a 6 day period




Genotype
MGI:4366843
cx5
Allelic
Composition
Bcl2tm1Dlo/Bcl2tm1Dlo
Bcl2l11tm1.1Ast/Bcl2l11+
Genetic
Background
B6.Cg-Bcl2tm1Dlo Bcl2l11tm1.1Ast
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl2l11tm1.1Ast mutation (4 available); any Bcl2l11 mutation (32 available)
Bcl2tm1Dlo mutation (0 available); any Bcl2 mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• spleens are heavier than those in homozygous Bcl-2 deficient mice
• more white blood cells numbers than in homozygous Bcl-2 deficient mice

immune system
• spleens are heavier than those in homozygous Bcl-2 deficient mice
• more white blood cells numbers than in homozygous Bcl-2 deficient mice

growth/size/body
• spleens are heavier than those in homozygous Bcl-2 deficient mice




Genotype
MGI:4366842
cx6
Allelic
Composition
Bcl2tm1Dlo/Bcl2tm1Dlo
Bcl2l11tm1.1Ast/Bcl2l11tm1.1Ast
Genetic
Background
B6.Cg-Bcl2tm1Dlo Bcl2l11tm1.1Ast
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl2l11tm1.1Ast mutation (4 available); any Bcl2l11 mutation (32 available)
Bcl2tm1Dlo mutation (0 available); any Bcl2 mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• spleens are much heavier than those in homozygous Bcl-2 deficient mice
• white blood cells numbers are much higher than in homozygous Bcl-2 deficient mice

immune system
• spleens are much heavier than those in homozygous Bcl-2 deficient mice
• white blood cells numbers are much higher than in homozygous Bcl-2 deficient mice

growth/size/body
• spleens are much heavier than those in homozygous Bcl-2 deficient mice




Genotype
MGI:4366834
cx7
Allelic
Composition
Bcl2tm1Dlo/Bcl2tm1Dlo
Bcl2l11tm1.1Boui/Bcl2l11tm1.1Boui
Genetic
Background
B6.Cg-Bcl2tm1Dlo Bcl2l11tm1.1Boui
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl2l11tm1.1Boui mutation (0 available); any Bcl2l11 mutation (32 available)
Bcl2tm1Dlo mutation (0 available); any Bcl2 mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

BH3 replacement mutations in Bcl2l11 prevent the development of polycystic kidney disease and spleen atrophy in Bcl2tm1Dlo/Bcl2tm1Dlo mice

growth/size/body

hematopoietic system
N
• normal splenic structure

immune system
N
• normal splenic structure

renal/urinary system
N
• mice do not develop polycystic kidney disease

pigmentation
• coat color becomes gray at 5 to 7 weeks of age

integument
• coat color becomes gray at 5 to 7 weeks of age




Genotype
MGI:4366840
cx8
Allelic
Composition
Bcl2tm1Dlo/Bcl2tm1Dlo
Bcl2l11tm1.1Boui/Bcl2l11tm2.1Boui
Genetic
Background
B6.Cg-Bcl2tm1Dlo Bcl2l11tm1.1Boui/Bcl2l11tm2.1Boui
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl2l11tm1.1Boui mutation (0 available); any Bcl2l11 mutation (32 available)
Bcl2l11tm2.1Boui mutation (0 available); any Bcl2l11 mutation (32 available)
Bcl2tm1Dlo mutation (0 available); any Bcl2 mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

BH3 replacement mutations in Bcl2l11 prevent the development of polycystic kidney disease and spleen atrophy in Bcl2tm1Dlo/Bcl2tm1Dlo mice

hematopoietic system
N
• normal splenic structure
• spleens are much heavier than those in homozygous Bcl-2 deficient mice
• spleens are much heavier than those in homozygous Bcl-2 deficient with only one Bcl2l1 deficient allele mice
• white blood cells numbers are six fold more abundant than in homozygous Bcl-2 deficient mice

renal/urinary system
N
• mice do not develop polycystic kidney disease

immune system
N
• normal splenic structure
• spleens are much heavier than those in homozygous Bcl-2 deficient mice
• spleens are much heavier than those in homozygous Bcl-2 deficient with only one Bcl2l1 deficient allele mice
• white blood cells numbers are six fold more abundant than in homozygous Bcl-2 deficient mice

growth/size/body
• spleens are much heavier than those in homozygous Bcl-2 deficient mice
• spleens are much heavier than those in homozygous Bcl-2 deficient with only one Bcl2l1 deficient allele mice




Genotype
MGI:4366836
cx9
Allelic
Composition
Bcl2tm1Dlo/Bcl2tm1Dlo
Bcl2l11tm2.1Boui/Bcl2l11tm2.1Boui
Genetic
Background
B6.Cg-Bcl2tm1Dlo Bcl2l11tm2.1Boui
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl2l11tm2.1Boui mutation (0 available); any Bcl2l11 mutation (32 available)
Bcl2tm1Dlo mutation (0 available); any Bcl2 mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

BH3 replacement mutations in Bcl2l11 prevent the development of polycystic kidney disease and spleen atrophy in Bcl2tm1Dlo/Bcl2tm1Dlo mice

growth/size/body

hematopoietic system
N
• normal splenic structure

immune system
N
• normal splenic structure

renal/urinary system
N
• mice do not develop polycystic kidney disease diluted coat color [MP:0000371]

pigmentation
• coat color becomes gray at 5 to 7 weeks of age

integument
• coat color becomes gray at 5 to 7 weeks of age




Genotype
MGI:4366837
cx10
Allelic
Composition
Bcl2tm1Dlo/Bcl2tm1Dlo
Bcl2l11tm3.1Boui/Bcl2l11tm3.1Boui
Genetic
Background
B6.Cg-Bcl2tm1Dlo Bcl2l11tm3.1Boui
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl2l11tm3.1Boui mutation (0 available); any Bcl2l11 mutation (32 available)
Bcl2tm1Dlo mutation (0 available); any Bcl2 mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

The Bcl2l11tm3.1Boui mutation ameliorates the degenerative disorders of Bcl2tm1Dlo/Bcl2tm1Dlo mice

mortality/aging
• live up to 300 days due to mild polycystic kidney disease (PKD)

growth/size/body
• mild signs of polycystic kidney disease (PKD)
• progress slowly
• live up to 300 days
• retarded growth
• most of these animals (n = 24) become healthy adults
• spleens are heavier than those in homozygous Bcl-2 deficient mice

hematopoietic system
N
• normal splenic structure
• less apoptosis than in homozygous Bcl-2 deficient mice spleen
• spleens are heavier than those in homozygous Bcl-2 deficient mice
• more white blood cells numbers than in homozygous Bcl-2 deficient mice

renal/urinary system
• mild signs of polycystic kidney disease (PKD)
• progress slowly
• live up to 300 days

immune system
N
• normal splenic structure
• less apoptosis than in homozygous Bcl-2 deficient mice spleen
• spleens are heavier than those in homozygous Bcl-2 deficient mice
• more white blood cells numbers than in homozygous Bcl-2 deficient mice

cellular
• less apoptosis than in homozygous Bcl-2 deficient mice spleen




Genotype
MGI:3612868
cx11
Allelic
Composition
Bcl2tm1Dlo/Bcl2tm1Dlo
Biktm1Ast/Biktm1Ast
Genetic
Background
B6.Cg-Bcl2tm1Dlo Biktm1Ast
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bcl2tm1Dlo mutation (0 available); any Bcl2 mutation (41 available)
Biktm1Ast mutation (1 available); any Bik mutation (11 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all homozygotes die from polycystic kidney disease between 2 and 4 weeks of age

growth/size/body
• all homozygotes die from polycystic kidney disease between 2 and 4 weeks of age
• all homozygotes become runted

immune system
• survival of mature resting T and B cells in the absence of cytokines is impaired compared to wild-type cells and similar to mice homozygous for Bcl2tm1Dlo alone

renal/urinary system
• all homozygotes die from polycystic kidney disease between 2 and 4 weeks of age

hematopoietic system
• survival of mature resting T and B cells in the absence of cytokines is impaired compared to wild-type cells and similar to mice homozygous for Bcl2tm1Dlo alone





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last database update
04/23/2024
MGI 6.23
The Jackson Laboratory