Abstract
During early postnatal development, a switch occurs between eEF1A-1/EF-1alpha and eEF1A-2/S1, homologous peptide elongation factors, in brain, heart, and skeletal muscle; eEF1A-2/S1 becomes the major form expressed in maturity. By immunofluorescent labeling, we detected both homologues in the developing brains of wild-type and wasted mutant mice, carrying a deletion in the eEF1A-2/S1 gene; we found that brain expression of eEF1A-2/S1 protein is restricted to mature, terminally differentiated neurons, and coincides with the disappearance of eEF1A-1/EF-1alpha 20 days after birth. Furthermore, no elongation factor 1A is present in wasted mutant mice neurons following the developmental switch, indicating that the genetic regulation silencing eEF1A-1/EF-1alpha is still functional.
Publication types
-
Comparative Study
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Animals
-
Animals, Newborn
-
Central Nervous System / cytology
-
Central Nervous System / growth & development*
-
Central Nervous System / metabolism*
-
Embryo, Mammalian
-
Fluorescent Antibody Technique / methods
-
Gene Expression Regulation, Developmental
-
Glial Fibrillary Acidic Protein / metabolism
-
Heterozygote
-
Mice
-
Mice, Inbred C57BL
-
Mice, Mutant Strains
-
Microscopy, Confocal / methods
-
Mutation
-
Neurofilament Proteins / metabolism
-
Neurons / metabolism
-
Peptide Elongation Factor 1 / genetics
-
Peptide Elongation Factor 1 / metabolism*
-
RNA, Messenger / biosynthesis
-
Reverse Transcriptase Polymerase Chain Reaction / methods
Substances
-
Eef1a2 protein, mouse
-
Glial Fibrillary Acidic Protein
-
Neurofilament Proteins
-
Peptide Elongation Factor 1
-
RNA, Messenger
-
neurofilament protein NF 68