A cytoplasmic suppressor of a nuclear mutation affecting mitochondrial functions in Drosophila.

ABSTRACT: Phenotypes relevant to oxidative phosphorylation (OXPHOS) in eukaryotes are jointly determined by nuclear and mitochondrial DNA (mtDNA). Thus, in humans, the variable clinical presentations of mitochondrial disease patients bearing the same primary mutation, whether in nuclear or mitochondrial DNA, have been attributed to putative genetic determinants carried in the "other" genome, though their identity and the molecular mechanism(s) by which they might act remain elusive. Here we demonstrate cytoplasmic suppression of the mitochondrial disease-like phenotype of the Drosophila melanogaster nuclear mutant tko(25t), which includes developmental delay, seizure sensitivity, and defective male courtship. The tko(25t) strain carries a mutation in a mitoribosomal protein gene, causing OXPHOS defi

SUBMITTER: Chen S 

PROVIDER: S-EPMC3454878 | biostudies-literature | 2012 Oct

REPOSITORIES: biostudies-literature