Selection and evolvability of mitochondrial traits in alpine swift (Tachymarptis melba)

Fundamental still-unanswered questions in evolutionary biology are related to the understanding of which mechanisms rule individual growth, reproduction, and survival (i.e., fitness). Mitochondria, also well-known as the powerhouse of the cell, are the organelles responsible for energy production in eukaryote cells through oxidative phosphorylation. It sets the efficiency to which food is converted into cellular energy, and thus how this energy is invested in fitness and overall maintenance. Mitochondrial functioning may be one of the key answers to explain individual heterogeneity in growth, reproduction, and survival. Oxidative phosphorylation produces up to 90% of the energy to fuel cell and therefore individuals. Thus, recent research suggested that variation in their functioning, efficiency and density might account for a large part of inter-individual differences in performance. Mitochondrial traits are also expected to show intra-individual variations and plasticity over the life course, depending on environmental such as parental care, diet, exposure to pollutants, or pathogen infections. The general objective of my PhD is to test how mitochondrial traits are selected and their potential evolvability across individuals and contexts, in a wild population of Alpine swift (Tachymarptis melba). Alpine swifts are caught in various colonies across Switzerland (Biel, Solothurn, Baden), where nestlings have been ringed for several decades and adults tracked since 1999. This long-term monitoring and the colonial nature of Alpine swift allows us to construct large pedigree over the years, establishing genetic link between offspring, parents, and the different colonies. Mitochondrial traits are measured is fresh blood samples within 24h after collection. The protocol is based on a substrate/inhibitor approach to quantify O2 consumption used for ATP synthesis (OXPHOS), and during mitochondrial proton leak (LEAK) through the inner mitochondrial membrane. Endogenous mitochondrial respiration (ROUTINE), maximal mitochondrial respiration (ETS) and non-mitochondrial respiration will also be measured. Other markers of oxidative stress (superoxide dismutase, glutathione, oxidative damage, antioxidant capacity, protein carbonyl, glucose), growth (IGF-1) and ageing (telomere length) will be measured to complete the physiological picture. The selection and evolvability of the traits will be determined with quantitative genetic approaches using animal models. In addition, various environmental factors will be introduced in our models, such as pollutants (metal trace elements, persistent organic pollutants) and pathogen prevalence (Trypanosoma sp. screening). At the end, we are expecting to depict what is the genetic architecture of mitochondrial traits in this natural bird population and what is the strength and direction of selection on mitochondrial traits (inter-individual variations). We are also interested in the potential turn-over of mitochondrial efficiency over the life-course (within-individual variations), also depending on environmental factors. Finally, we aim to investigate what are the causal cascading effects of changes in mitochondrial function on reproduction or survival.