Open AccessThe 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
Author(s) -
D. Chambers,
Josephine Peters,
Catherine M. Abbott
Publication year - 1998
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.95.8.4463
Subject(s) - biology , gene isoform , elongation factor , mutation , phenotype , gene , microbiology and biotechnology , genetics , locus (genetics) , translation (biology) , eukaryotic translation , eukaryotic translation elongation factor 1 alpha 1 , messenger rna , rna , ribosome
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 calledEef1a2 , encoding a protein that is 92% identical at the amino acid level to the translation elongation factor EF1α (locusEef1a ). We have found no evidence for the involvement of another gene in this deletion. Expression ofEef1a2 is reciprocal with that ofEef1a . Expression ofEef1a2 takes over fromEef1a 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.