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Haploinsufficiency for translation elongation factor eEF1A2 in aged mouse muscle and neurons is compatible with
Lowri A Griffiths1, Jennifer Doig, Antonia M D Churchhouse
1Centre for Molecular Medicine, Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom.
Plos One
|August 1, 2012
Summary
Heterozygous mice with reduced translation elongation factor eEF1A2 expression show no signs of neurodegeneration or muscle wasting, even when aged. This suggests that a 50% reduction in eEF1A2 is compatible with normal function.
Area of Science:
- Neuroscience
- Genetics
- Molecular Biology
Background:
- The translation elongation factor isoform eEF1A2 is crucial for muscle and neuron function.
- Deletion of eEF1A2 causes the
- wasted
- (wst) phenotype in mice, leading to muscle wasting and neurodegeneration.
- Heterozygous models of neurodegenerative diseases can exhibit subtle phenotypes.
Purpose of the Study:
- To investigate the effects of aging on heterozygous +/wst mice with reduced eEF1A2 expression.
- To determine if a 50% reduction in eEF1A2 is compatible with normal neuromuscular function and spinal cord health.
- To assess potential subtle phenotypic abnormalities in aged heterozygous mice.
Main Methods:
- Grip strength assay to evaluate neuromuscular function in young and aged mice.
- Rotarod performance test to assess motor coordination and balance.
- Immunohistochemistry of spinal cord sections to examine neuropathology.
Main Results:
- Aged heterozygous +/wst mice exhibited no deficits in grip strength or rotarod performance compared to wild-type controls.
- No signs of spinal cord pathology were observed in aged heterozygous mice.
- Despite reduced eEF1A2 levels, heterozygous mice maintained normal neuromuscular function throughout aging.
Conclusions:
- A 50% reduction in eEF1A2 expression is compatible with normal neuromuscular function and spinal cord integrity during aging.
- The
- wasted
- mutation in eEF1A2 does not appear to cause a significant phenotype in heterozygous mice.
- Further research may be needed to understand the precise role of eEF1A2 dosage in neurodegenerative processes.
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