Phenotypes associated with this allele

• Allele Symbol: Cntf^tm1Mpin
• Allele Name: targeted mutation 1, Max-Planck-Institute for Neurobiology
• Allele ID: MGI:1857773
• Summary: 4 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Cntf^tm1Mpin/Cntf^tm1Mpin	B6.129S2-Cntf^tm1Mpin	MGI:5298862
hm2	Cntf^tm1Mpin/Cntf^tm1Mpin	involves: 129S2/SvPas	MGI:3618312
hm3	Cntf^tm1Mpin/Cntf^tm1Mpin	involves: 129S2/SvPas * C57BL/6	MGI:5298863
cx4	Cntf^tm1Mpin/Cntf^tm1Mpin Lif^tm1Phb/Lif^tm1Phb	involves: 129S2/SvPas * C57BL/6	MGI:5298864

Genotype
MGI:5298862

hm1

• Allelic Composition: Cntf^tm1Mpin/Cntf^tm1Mpin
• Genetic Background: B6.129S2-Cntf^tm1Mpin

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

nervous system

decreased oligodendrocyte progenitor number ( J:126852 )

• in MOG33-35-treated mice

abnormal oligodendrocyte apoptosis ( J:126852 )

• increased in MOG33-35-treated mice

abnormal myelin sheath morphology ( J:126852 )

• severe vascular dystrophy of myelin in MOG33-35-treated mice

axon degeneration ( J:126852 )

• in MOG33-35-treated mice

immune system

increased susceptibility to experimental autoimmune encephalomyelitis ( J:126852 )

• 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

decreased oligodendrocyte progenitor number ( J:126852 )

• in MOG33-35-treated mice

abnormal oligodendrocyte apoptosis ( J:126852 )

• increased in MOG33-35-treated mice

Genotype
MGI:3618312

hm2

• Allelic Composition: Cntf^tm1Mpin/Cntf^tm1Mpin
• Genetic Background: involves: 129S2/SvPas

nervous system

abnormal microglial cell morphology ( J:15313 )

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

abnormal motor neuron morphology ( J:15313 )

• 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

decreased motor neuron number ( J:15313 )

• 22% reduction in facial motor neurons at 28 weeks of age but not at 4 weeks of age

motor neuron degeneration ( J:15313 )

• 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

muscle weakness ( J:15313 )

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

behavior/neurological

decreased grip strength ( J:15313 )

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

hematopoietic system

abnormal microglial cell morphology ( J:15313 )

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

immune system

abnormal microglial cell morphology ( J:15313 )

• 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: Cntf^tm1Mpin/Cntf^tm1Mpin
• Genetic Background: involves: 129S2/SvPas * C57BL/6

homeostasis/metabolism

increased susceptibility to injury ( J:84375 , J:158286 )

• 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

nervous system phenotype ( J:141582 )

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

N • mice exhibit normal induction of nerve terminal sprouting, reactivation of terminal Schwann cells, and compensatory reinnervation after nerve injury

abnormal axon extension ( J:158286 )

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

abnormal astrocyte physiology ( J:84375 )

• stronger activation following optic nerve crush injury

cellular

abnormal axon extension ( J:158286 )

• 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: Cntf^tm1Mpin/Cntf^tm1Mpin; Lif^tm1Phb/Lif^tm1Phb
• Genetic Background: involves: 129S2/SvPas * C57BL/6

nervous system

abnormal axon extension ( J:158286 )

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

homeostasis/metabolism

increased susceptibility to injury ( J:158286 )

• 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

abnormal axon extension ( J:158286 )

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