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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Cntftm1Mpin
targeted mutation 1, Max-Planck-Institute for Neurobiology
MGI:1857773
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Cntftm1Mpin/Cntftm1Mpin B6.129S2-Cntftm1Mpin MGI:5298862
hm2
Cntftm1Mpin/Cntftm1Mpin involves: 129S2/SvPas MGI:3618312
hm3
Cntftm1Mpin/Cntftm1Mpin involves: 129S2/SvPas * C57BL/6 MGI:5298863
cx4
Cntftm1Mpin/Cntftm1Mpin
Liftm1Phb/Liftm1Phb
involves: 129S2/SvPas * C57BL/6 MGI:5298864


Genotype
MGI:5298862
hm1
Allelic
Composition
Cntftm1Mpin/Cntftm1Mpin
Genetic
Background
B6.129S2-Cntftm1Mpin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cntftm1Mpin mutation (1 available); any Cntf mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• in MOG33-35-treated mice
• increased in MOG33-35-treated mice
• severe vascular dystrophy of myelin in MOG33-35-treated mice
• in MOG33-35-treated mice

immune system
• mice treated with MOG33-35 exhibit more severe experimental autoimmune encephalomyelitis with decreased oligodendrocyte precursor cells, increased oligodendrocyte apoptosis, and severe vacuolar dystrophy of myelin and axonal damage compared with wild-type mice

cellular
• in MOG33-35-treated mice
• increased in MOG33-35-treated mice




Genotype
MGI:3618312
hm2
Allelic
Composition
Cntftm1Mpin/Cntftm1Mpin
Genetic
Background
involves: 129S2/SvPas
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cntftm1Mpin mutation (1 available); any Cntf mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• atrophic and degenerative changes in spinal motor neurons are accompanied by an increase in the numbers of activated microglial cells
• at 8 weeks of age, lumbar motor neuron cell bodies are smaller and the nuclei are swollen, resulting in an increase in the ratio between nuclear and cytoplasmic areas of about 40%, however by 14 weeks of age, both cell area and nuclear area are smaller
• 22% reduction in facial motor neurons at 28 weeks of age but not at 4 weeks of age
• with increasing age, spinal motor neurons exhibit progressive atrophy and finally degeneration
• trophy becomes apparent by 8 weeks of age and the first signs of degeneration are seen at 22 weeks of age

muscle
• small but significant reduction in muscle strength at 28 weeks of age, as indicated by forelimb grip strength

behavior/neurological
• small but significant reduction in forelimb grip strength at 28 weeks of age

hematopoietic system
• atrophic and degenerative changes in spinal motor neurons are accompanied by an increase in the numbers of activated microglial cells

immune system
• atrophic and degenerative changes in spinal motor neurons are accompanied by an increase in the numbers of activated microglial cells




Genotype
MGI:5298863
hm3
Allelic
Composition
Cntftm1Mpin/Cntftm1Mpin
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cntftm1Mpin mutation (1 available); any Cntf mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• following optic nerve crush injury, mice exhibit stronger activation of astrocytes compared with wild-type mice (J:84375)
• after optic nerve crush and or lens injury, axotomized retinal ganglion cells exhibit reduced neurite outgrowth and reduced axon regeneration compared with wild-type cells (J:158286)
• however, retinal ganglion cell survival after injury is normal (J:158286)

nervous system
N
• mice exhibit extensive terminal sprouting in response to major sprouting-stimuli (CNTF, botulinum toxin-elicited paralysis, and partial denervation by L4 spinal root transection) with normal numbers, length, and growth patterns of terminal sprouts, and extent of reinnervation by terminal or nodal sprouts
• mice exhibit normal induction of nerve terminal sprouting, reactivation of terminal Schwann cells, and compensatory reinnervation after nerve injury
• after optic nerve crush and or lens injury, axotomized retinal ganglion cells exhibit reduced neurite outgrowth compared with wild-type cells
• stronger activation following optic nerve crush injury

cellular
• after optic nerve crush and or lens injury, axotomized retinal ganglion cells exhibit reduced neurite outgrowth compared with wild-type cells




Genotype
MGI:5298864
cx4
Allelic
Composition
Cntftm1Mpin/Cntftm1Mpin
Liftm1Phb/Liftm1Phb
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cntftm1Mpin mutation (1 available); any Cntf mutation (13 available)
Liftm1Phb mutation (0 available); any Lif mutation (11 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
nervous system
• after optic nerve crush and lens injury, axotomized retinal ganglion cells fail to exhibit neurite outgrowth unlike with wild-type cells

homeostasis/metabolism
• after optic nerve crush and lens injury, axotomized retinal ganglion cells fail to exhibit neurite outgrowth unlike with wild-type cells and reduced axon regeneration compared with wild-type cells
• however, retinal ganglion cell survival after injury is normal

cellular
• after optic nerve crush and lens injury, axotomized retinal ganglion cells fail to exhibit neurite outgrowth unlike with wild-type cells





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