A mitochondrial DNA hypomorph of cytochrome oxidase specifically impairs male fertility in Drosophila melanogaster

Due to their strict maternal inheritance in most animals and plants, mitochondrial genomes are predicted to accumulate mutations that are beneficial or neutral in females but harmful in males. Although a few male-harming mtDNA mutations have been identified, consistent with this 'Mother's...

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Bibliographic Details
Published in:eLife 2016-08, Vol.5
Main Authors: Patel, Maulik R, Miriyala, Ganesh K, Littleton, Aimee J, Yang, Heiko, Trinh, Kien, Young, Janet M, Kennedy, Scott R, Yamashita, Yukiko M, Pallanck, Leo J, Malik, Harmit S
Format: Article
Language:English
Subjects:
Animals
Cell Biology
Cytochrome oxidase II
Cytochromes
DNA sequencing
DNA, Mitochondrial - genetics
Drosophila
Drosophila melanogaster
Drosophila melanogaster - genetics
Drosophila melanogaster - physiology
Electron Transport Complex IV - genetics
experimental evolution
Females
Fertility
Gametogenesis
Genetic aspects
genetic suppressors
Genomes
Genomics and Evolutionary Biology
Infertility
Infertility - genetics
lifespan
Male
male fertility
Males
Maternal inheritance
Medical research
Methods
Mitochondria
Mitochondrial DNA
Mitochondrial Proteins - genetics
Motility
Mutation
Mutation, Missense
Nucleotide sequencing
Phosphorylation
Physiological aspects
Sperm
sperm development
Sterility
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Summary:Due to their strict maternal inheritance in most animals and plants, mitochondrial genomes are predicted to accumulate mutations that are beneficial or neutral in females but harmful in males. Although a few male-harming mtDNA mutations have been identified, consistent with this 'Mother's Curse', their effect on females has been largely unexplored. Here, we identify COII(G177S), a mtDNA hypomorph of cytochrome oxidase II, which specifically impairs male fertility due to defects in sperm development and function without impairing other male or female functions. COII(G177S) represents one of the clearest examples of a 'male-harming' mtDNA mutation in animals and suggest that the hypomorphic mtDNA mutations like COII(G177S) might specifically impair male gametogenesis. Intriguingly, some D. melanogaster nuclear genetic backgrounds can fully rescue COII(G177S) -associated sterility, consistent with previously proposed models that nuclear genomes can regulate the phenotypic manifestation of mtDNA mutations.
ISSN:2050-084X
2050-084X
DOI:10.7554/eLife.16923