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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Abl2tm1Ajk
targeted mutation 1, Anthony J Koleske
MGI:2153719
Summary 8 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Abl2tm1Ajk/Abl2tm1Ajk involves: 129S4/SvJae MGI:3583884
hm2
Abl2tm1Ajk/Abl2tm1Ajk involves: 129S4/SvJae * C57BL/6J MGI:2653884
cn3
Abl1tm2.1Goff/Abl1tm2.1Goff
Abl2tm1Ajk/Abl2tm1Ajk
Tg(Nes-cre)1Kln/0
involves: 129 * C57BL/6 * C57BL/6J * SJL MGI:4850044
cn4
Abl1tm2.1Goff/Abl1tm2.1Goff
Abl2tm1Ajk/Abl2tm1Ajk
Tg(Atoh1-cre)1Bfri/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J * CBA MGI:4850045
cn5
Abl1tm1Ajk/Abl1tm1Ajk
Abl2tm1Ajk/Abl2tm1Ajk
Tg(Nes-cre)1Kag/?
involves: 129S4/SvJae MGI:3583883
cx6
Abl1tm1Mlg/Abl1tm1Mlg
Abl2tm1Ajk/Abl2+
involves: 129S/SvEv * 129S4/SvJae * C57BL/6J MGI:2653892
cx7
Abl1tm1Mlg/Abl1+
Abl2tm1Ajk/Abl2tm1Ajk
involves: 129S/SvEv * 129S4/SvJae * C57BL/6J MGI:2653894
cx8
Abl1tm1Mlg/Abl1tm1Mlg
Abl2tm1Ajk/Abl2tm1Ajk
involves: 129S/SvEv * 129S4/SvJae * C57BL/6J MGI:2653897


Genotype
MGI:3583884
hm1
Allelic
Composition
Abl2tm1Ajk/Abl2tm1Ajk
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abl2tm1Ajk mutation (0 available); any Abl2 mutation (79 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• smaller dendrite arbors resulting in more densely packed neurons in all layers of cortex in 6-8 weeks old mice




Genotype
MGI:2653884
hm2
Allelic
Composition
Abl2tm1Ajk/Abl2tm1Ajk
Genetic
Background
involves: 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abl2tm1Ajk mutation (0 available); any Abl2 mutation (79 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• pups weigh about 80% of wild-type at 3 weeks of age, however by 8 weeks of age, weight does not differ from wild-type

behavior/neurological
• at 5 weeks of age, some mutants show increased tendency for retropulsion (walking backward) when placed in an open test field, however they are as active as littermate controls
• males display decreased aggression towards intruding mice
• most mutants are not startled by acoustic stimuli
• the magnitude of the startle responses of the few mutants that respond to an acoustic stimuli is only about 30% of the magnitude of controls
• mutants respond only slightly less well than controls to tactile (air puff) startle stimuli
• poor performance on rope climbing test
• however, mutants are not ataxic, do not exhibit altered gait, and they are able to remain upright when walking on a narrow suspended platform
• mutants spend less time hanging from a wire bar cage lid than controls

reproductive system
• mutants produce litters at a reduced frequency, however litter sizes are normal




Genotype
MGI:4850044
cn3
Allelic
Composition
Abl1tm2.1Goff/Abl1tm2.1Goff
Abl2tm1Ajk/Abl2tm1Ajk
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abl1tm2.1Goff mutation (1 available); any Abl1 mutation (92 available)
Abl2tm1Ajk mutation (0 available); any Abl2 mutation (79 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• recovered at a frequency (20.5%) slightly less than the expected Mendelian ratio at two weeks of age

nervous system
• reduced number of proliferating granule cell precursors (GCPs) in the secondary fissure in the posterior cerebellum at P8
• loss of proliferating GCPs is concentrated in areas where the basement membrane (BM) is disrupted
• normal proliferation of GCPs in the cerebella-derived culture
• scores of granule cell precursors (GCPs) abnormally protrude into the subarachnoid space between the midbrain and cerebellum at E17
• laminin-labeled basement membrane (BM) is fragmented at E15 and E17
• loss of the pial BM in the cerebellum starting from around P8
• reduced anterior-posterior extent of the mutant adult cerebellum
• basic laminar structure of the anterior cerebellum, encompassing lobules I-V, is completely lost
• obvious defects in the organization of anterior lobules I-V in P7 and P1 cerebella
• adjacent lobules, such as lobules VIII and IX, are fused
• patches of granule cells are randomly scattered throughout the white matter
• abnormal Bergmann glial network correlates with breaches of the BM in the cerebellum at P8
• highly disorganized radial glial processes, with some of their endfeet protruding into the meninges in the mutant cerebellum at E15
• loosely aligned Purkinje cells, with some abnormally distributing at the cerebellar surface at P1
• GCPs ectopically embed within the cortex at P1
• ectopic granule cell differentiation near the broken BM at P8
• many granule cells ectopias at the cerebellar surface in the posterior regions of adult cerebella and along the fusion lines of adjacent lobules
• normal extent of migration of granule cells and granule cell-glia interactions at P10 before the loss of the BM
• decreased depth of the fissures
• both the cerebellar vermis and the two lateral hemispheres lack clear fissures on the surface
• disappearance of lobules IV and V in the anterior vermis
• smaller cerebellum in adult mice

behavior/neurological
• take approximately twice as long to cross the elevated balance beam
• dramatic increase in the number of foot slips

cellular
• reduced number of proliferating granule cell precursors (GCPs) in the secondary fissure in the posterior cerebellum at P8
• loss of proliferating GCPs is concentrated in areas where the basement membrane (BM) is disrupted
• normal proliferation of GCPs in the cerebella-derived culture




Genotype
MGI:4850045
cn4
Allelic
Composition
Abl1tm2.1Goff/Abl1tm2.1Goff
Abl2tm1Ajk/Abl2tm1Ajk
Tg(Atoh1-cre)1Bfri/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abl1tm2.1Goff mutation (1 available); any Abl1 mutation (92 available)
Abl2tm1Ajk mutation (0 available); any Abl2 mutation (79 available)
Tg(Atoh1-cre)1Bfri mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
N
• normal cerebella




Genotype
MGI:3583883
cn5
Allelic
Composition
Abl1tm1Ajk/Abl1tm1Ajk
Abl2tm1Ajk/Abl2tm1Ajk
Tg(Nes-cre)1Kag/?
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abl1tm1Ajk mutation (1 available); any Abl1 mutation (92 available)
Abl2tm1Ajk mutation (0 available); any Abl2 mutation (79 available)
Tg(Nes-cre)1Kag mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• only 35% of the expected Mendelian numbers are born
• those that were born survived well into adulthood

nervous system
• smaller dendrite arbors resulting in more densely packed neurons in all layers of cortex in 6-8 weeks old mice




Genotype
MGI:2653892
cx6
Allelic
Composition
Abl1tm1Mlg/Abl1tm1Mlg
Abl2tm1Ajk/Abl2+
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abl1tm1Mlg mutation (2 available); any Abl1 mutation (92 available)
Abl2tm1Ajk mutation (0 available); any Abl2 mutation (79 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

cardiovascular system
• seen in most mutants
• the pericardial sac of many mutants is enlarged and edematous
• seen in most mutants

growth/size/body
• the peritoneum of many mutants is enlarged and edematous

homeostasis/metabolism
• seen in most mutants
• peritoneum is edematous in many mutants




Genotype
MGI:2653894
cx7
Allelic
Composition
Abl1tm1Mlg/Abl1+
Abl2tm1Ajk/Abl2tm1Ajk
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abl1tm1Mlg mutation (2 available); any Abl1 mutation (92 available)
Abl2tm1Ajk mutation (0 available); any Abl2 mutation (79 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• only 60% of the expected numbers of mutants are recovered postnatally

growth/size/body
• survivors are runted at birth, however they survive well into adulthood




Genotype
MGI:2653897
cx8
Allelic
Composition
Abl1tm1Mlg/Abl1tm1Mlg
Abl2tm1Ajk/Abl2tm1Ajk
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Abl1tm1Mlg mutation (2 available); any Abl1 mutation (92 available)
Abl2tm1Ajk mutation (0 available); any Abl2 mutation (79 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

nervous system
• mutants exhibit delayed appearance of Map2-positive early neurons in the neuroepithelium
• neuroepithelial cells show alterations in actin cytoskeleton
• the neuroepithelium collapses into the lumen of the neural tube at E10.25
• delay of neural tube closure is seen at E9.5, with the neural tube of most embryos closed by E10.25, although in some embryos, gaps remain at one or more fusion points in the head region

cellular
• neuroepithelial cells show alterations in actin cytoskeleton
• embryos from E10.5-E11 have massive numbers of apoptotic cells in all tissues of the body
• mutants exhibit delayed appearance of Map2-positive early neurons in the neuroepithelium

cardiovascular system

embryo
• embryos from E10.5-E11 have massive numbers of apoptotic cells in all tissues of the body
• neuroepithelial cells show alterations in actin cytoskeleton
• the neuroepithelium collapses into the lumen of the neural tube at E10.25
• delay of neural tube closure is seen at E9.5, with the neural tube of most embryos closed by E10.25, although in some embryos, gaps remain at one or more fusion points in the head region

homeostasis/metabolism





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