B7 From genotype to phenotype – linking the evolution of the mitochondrial OXPHOS system, mitochondrial capacity, metabolic rates and hybrid incompatibility in the parasitoid wasp Nasonia

The project aims to understand the genomic, genetic and physiological basis of nuclear cytoplasmic incompatibilities, specifically concerning mitochondria. Well-functioning mitochondria are essential for the survival and reproduction of all eukaryotes, including humans. To make a functioning mitochondrion, both nuclear and mitochondrial genes have to interact harmoniously. In general, mitochondrial genomes evolve faster, posing a potential problem due to nuclear cytoplasmic incompatibilities. In humans, mitochondrial mutations cause the most common human genetic diseases. Additionally, nuclear-cytoplasmic incompatibilities contribute to early postzygotic isolation between incipient species.

This project uses known hybrid incompatibilities in a four-species parasitoid wasp system to reveal and understand the genetic architecture of the observed nuclear-cytoplasmic incompatibilities in F2 male hybrids. This incompatibility comes in degrees ranging from none to 90% lethality in the most distant crosses. It is also known that rearing temperature influences the effect of this hybrid incompatibility (e.g., no offspring survive at 15°C and 31°C, but >30% survive at 25°C for one cross). Hence, we will investigate the interaction of temperature, nuclear-cytoplasmic incompatibilities and mitochondrial evolution. This should help us to generally identify and understand the gene regulatory networks that allow the nuclear and mitochondrial encoded genes to interact appropriately.