Mitochondria play a key role in energy metabolism through cellular respiration and provision of carbon skeletons for biosynthetic pathways, and act as gatekeepers for stress and cell death pathways such as apoptosis. The balance of these processes depends on the correct interaction between two different genomes, the mitochondrial and the nuclear genomes. As demonstrated by hybridization events, the cost of mitonuclear mismatches is metabolic dysfunction and potentially severe fitness loss. Temperature and dietary regimes are also well-known metabolic stressors influencing mitochondrial functions, metabolomic network structure and gene expression. Hence their variation can exacerbate mitonuclear incompatibilities.
Understanding the ability of animals to face the potential modification of their habitats is of vital importance. Climate change predictions estimate an increase in temperature and its variability, changes in in food web structures and in the distribution of populations. Events that may generate mitonuclear mismatches (such as hybridization between separate populations) are therefore expected to increase in frequency following the shifts in thermal niches.
The objective of this research is to test how far mitonuclear interactions contribute to thermal and dietary adaptation or breakdown in changing environments. Drosophila melanogaster is a leading model system to examine mito-nuclear interactions and adaptation. I will specifically employ experimental fly lines characterized by mitonuclear match and mismatch to investigate how temperature and diet modulation impact the major fitness effects of mitonuclear incompatibilities. This will be tested at the level of mitochondrial functions, gene expression and life-history trade-offs. The proposed project will be unique in its field, providing fundamental insights into how genetic and environmental factors interactions might translate to ecological population dynamics in a mutating world.
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