TitlePhenotypic rescue by a bovine transgene in a Cu/Zn superoxide dismutase-null mutant of Drosophila melanogaster.
Publication TypeJournal Article
Year of Publication1994
AuthorsReveillaud I, Phillips J, Duyf B, Hilliker A, Kongpachith A, Fleming JE
JournalMol Cell Biol
Volume14
Issue2
Pagination1302-7
Date Published1994 Feb
ISSN0270-7306
KeywordsAnimals, Animals, Genetically Modified, Cattle, Crosses, Genetic, Drosophila melanogaster, Electrophoresis, Polyacrylamide Gel, Female, Fertility, Infertility, Male, Isoenzymes, Longevity, Male, Phenotype, Superoxide Dismutase, X Chromosome
Abstract

Null mutants for Cu/Zn superoxide dismutase (CuZnSOD) in Drosophila melanogaster are male sterile, have a greatly reduced adult life span, and are hypersensitive to paraquat. We have introduced a synthetic bovine CuZnSOD transgene under the transcriptional control of the D. melanogaster 5C actin promoter into a CuZnSOD-null mutant of D. melanogaster. This was carried out by P-element-mediated transformation of the Drosophila-bovine CuZnSOD transgene into a CuZnSOD+ recipient strain followed by genetic crossing of the transgene into a strain carrying the CuZnSOD-null mutation, cSODn108. The resulting transformants express bovine CuZnSOD exclusively to about 30% of normal Drosophila CuZnSOD levels. Expression of the Drosophila-bovine CuZnSOD transgene in the CuZnSOD-null mutant rescues male fertility and resistance to paraquat to apparently normal levels. However, adult life span is restored to only 30% of normal, and resistance to hyperoxia is 90% of that found in control flies. This striking differential restoration of pleiotropic phenotypes could be the result of a threshhold of CuZnSOD expression necessary for normal male fertility and resistance to the toxicity of paraquat or hyperoxia which is lower than the threshold required to sustain a normal adult life span. Alternatively, the differential rescue of fertility, resistance to active oxygen, and life span might indicate different cell-specific transcriptional requirements for these functions which are normally provided by the control elements of the native CuZnSOD gene but are only partly compensated for by the transcriptional control elements of the actin 5C promoter.

DOI10.1128/mcb.14.2.1302
Alternate JournalMol. Cell. Biol.
PubMed ID8289809
PubMed Central IDPMC358485