Phenotypes associated with this allele

• Allele Symbol: Gas7^tm1Slch
• Allele Name: targeted mutation 1, Sue Lin-Chao
• Allele ID: MGI:5702632
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Gas7^tm1Slch/Gas7^tm1Slch	B6.129-Gas7^tm1Slch	MGI:5707621

Genotype
MGI:5707621

hm1

• Allelic Composition: Gas7^tm1Slch/Gas7^tm1Slch
• Genetic Background: B6.129-Gas7^tm1Slch

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

The number of motor neurons is decreased in old Gas7^tm1Slch/Gas7^tm1Slch mice

behavior/neurological

impaired coordination ( J:227375 )

• in a rotarod test, aged (12-15 months), but not adult (3-6 months), homozygotes perform significantly worse than wild-type controls at either accelerating speed or constant velocity

• however, stride analysis revealed so signs of ataxia or abnormal walking gait

decreased grip strength ( J:227375 )

• aged, but not adult, homozygotes show significantly reduced hanging ability from a horizontal bar or cage wire relative to wild-type controls

nervous system

nervous system phenotype ( J:227375 )

N • at 12 months of age, homozygotes show normal gross neuronal architecture and morphology in the cortex, hippocampus, and cerebellum

decreased motor neuron number ( J:227375 )

• at 12, but not at 3 months of age, choline acetyltransferase (ChAT) staining revealed a significant reduction in the average number of spinal motor neurons in the ventral horn relative to wild-type controls

abnormal neuromuscular synapse morphology ( J:227375 )

• aged homozygotes display ~30% of NMJs with axon terminal sprouts relative to 60% in age-matched wild-type controls

• however, the number of major nerve terminal branches per NMJ is not significantly altered

abnormal motor nerve collateral sprouting ( J:227375 )

• aged homozygotes exhibit an impaired ability to compensate for motor neuron loss by axon terminal sprouting

• the % of neuromuscular junctions (NMJs) exhibiting axon terminal sprouts is about half of that in wild-type controls

muscle

abnormal soleus morphology ( J:227375 )

• at 3 months of age, homozygotes show a mild increase in MHCI (slow muscle fiber) protein levels in the soleus relative to age-matched wild-type controls

• at 12 months of age, homozygotes display lower MHC II (fast muscle fiber) and higher MHC I (slow muscle fiber) protein levels in the soleus relative to age-matched controls

increased skeletal muscle fiber diameter ( J:227375 )

• in the soleus muscle, aged homozygotes show a slight increase in the median cross-sectional area of slow muscle fibers relative to age-matched wild-type controls

• however, no such change is observed in the soleus fast muscle fibers

abnormal skeletal muscle fiber type ratio ( J:227375 )

• in the soleus muscle, aged homozygotes show a significantly lower ratio of fast to slow muscle fibers (1:1) than age-matched wild-type controls (~3:2)

• however, muscle fiber subtype composition is normal in the extensor digitorum longus (EDL) muscle

progressive muscle weakness ( J:227375 )

• homozygotes exhibit loss of muscle strength during aging, as measured by hanging time on a horizontal bar or cage wire

growth/size/body

growth/size/body region phenotype ( J:227375 )

N • adult and aged male and female homozygotes display normal body weights relative to age-matched wild-type controls

limbs/digits/tail

abnormal soleus morphology ( J:227375 )

• at 3 months of age, homozygotes show a mild increase in MHCI (slow muscle fiber) protein levels in the soleus relative to age-matched wild-type controls

• at 12 months of age, homozygotes display lower MHC II (fast muscle fiber) and higher MHC I (slow muscle fiber) protein levels in the soleus relative to age-matched controls