Haploinsufficiency for translation elongation factor eEF1A2 in aged mouse muscle and neurons is compatible with normal function.

摘要: Translation elongation factor isoform eEF1A2 is expressed in muscle and neurons. Deletion of mice gives rise to the neurodegenerative phenotype “wasted” (wst). Mice homozygous for wasted mutation die wasting neurodegeneration at four weeks post-natal. Although said be recessive, aged heterozygous have never been examined detail; a number other mouse models motor neuron degeneration recently shown similar, albeit less severe, phenotypic abnormalities state. We therefore effects ageing on cohort +/wst control mice, order establish whether presumed 50% reduction expression was compatible with normal function. evaluated grip strength assay as way distinguishing between wild-type 3–4 weeks, then performed same older mice. also used rotarod performance immunohistochemistry spinal cord sections evaluate Heterozygous mutant showed no deficit neuromuscular function or signs pathology, spite low levels eEF1A2.