Causes and Consequences of Hybrid Incompatibilities in Arabidopsis thaliana

Abstract

Gardeners, farmers, natural scientists and Augustinian monks alike have long been interested in the study of plant hybrids. And why not - the study of hybridization has taught us much about variation and the fodder that it provides for evolution. The first chapter of my thesis begins, therefore, with a brief history of the study of hybridization. I describe some of the key concepts and examples that have shaped our understanding of evolution and speciation. Crosses between populations of the same species often uncover transgressive phenotypes in the progeny that were not present in the parents. These phenotypes may be advantageous or deleterious for the progeny, and in the latter case may serve to prevent interbreeding of the two populations. Different geographic populations may be exposed to different environments such as temperature, nutrient availability and pathogen pressure. The study of hybrid incompatibilities, therefore, helps us to determine both the mechanisms that lead to such incompatibilities and the role played by the environment in this divergence. One such incompatibility is hybrid necrosis. It is a temperature dependent phenomenon caused by an overactive immune system. In Chapter 3 of my thesis, I describe the reaction norms of this autoimmunity with respect to temperature. Mine was the first systematic study of the molecular and morphological phenotypes associated with hybrid necrosis at a range of temperatures. Activation of the immune system usually entails a cost to growth. However, by assaying both immunity genes and plant biomass, I show that there are points in the temperature gradient where this see-saw between growth and defense can be balanced. In Chapter 4 of my thesis, I describe a newly discovered hybrid phenotype. F1 hybrids displayed an altered shoot architecture characterised by a loss of apical dominance and a bushy habit. Hybrids of the F2 generation showed an additional, segregating phenotype of increased anthocyanin accumulation and small stature. I describe the genetic basis of this hybrid incompatibility in part and show that the two seemingly different phenotypes are linked genetically. One of the genes that I identified to be involved in this hybrid incompatibility is a microtubule-associated protein. This family of proteins has never before been associated with the phenotypes that I describe. Therefore, further study of this incompatibility is expected to detail new pathways regulating shoot architecture and anthocyanin accumulation.