The lethal mutation of the mouse wasted ( wst ) is a deletion that abolishes expression of a tissue-specific isoform of translation elongation factor 1α, encoded by the Eef1a2 gene
Copyright policy )The lethal mutation of the mouse wasted ( wst ) is a deletion that abolishes expression of a tissue-specific isoform of translation elongation factor 1α, encoded by the Eef1a2 gene
We have identified the mutation responsible for the autosomal recessive wasted ( wst ) mutation of the mouse. Wasted mice are characterized by wasting and neurological and immunological abnormalities starting at 21 days after birth; they die by 28 days. A deletion of 15.8 kb in wasted mice abolishes expression of a gene called Eef1a2 , encoding a protein that is 92% identical at the amino acid level to the translation elongation factor EF1α (locus Eef1a ). We have found no evidence for the involvement of another gene in this deletion. Expression of Eef1a2 is reciprocal with that of Eef1a . Expression of Eef1a2 takes over from Eef1a in heart and muscle at precisely the time at which the wasted phenotype becomes manifest. These data suggest that there are tissue-specific forms of the translation elongation apparatus essential for postnatal survival in the mouse.
- NHS Lothian United Kingdom
- Imperial College Healthcare NHS Trust United Kingdom
- Medical Research Council United Kingdom
- University of Edinburgh United Kingdom
- Western General Hospital United Kingdom
Aging, Base Sequence, Myocardium, Molecular Sequence Data, Gene Expression Regulation, Developmental, Genes, Recessive, Mice, Inbred Strains, Exons, Peptide Elongation Factors, Polymerase Chain Reaction, Mice, Mutant Strains, Mice, Peptide Elongation Factor 1, Sequence Homology, Nucleic Acid, Animals, Genes, Lethal, Promoter Regions, Genetic, Chromosomes, Artificial, Yeast, Sequence Alignment, Sequence Deletion
Aging, Base Sequence, Myocardium, Molecular Sequence Data, Gene Expression Regulation, Developmental, Genes, Recessive, Mice, Inbred Strains, Exons, Peptide Elongation Factors, Polymerase Chain Reaction, Mice, Mutant Strains, Mice, Peptide Elongation Factor 1, Sequence Homology, Nucleic Acid, Animals, Genes, Lethal, Promoter Regions, Genetic, Chromosomes, Artificial, Yeast, Sequence Alignment, Sequence Deletion
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