Selfish genetic elements increase their transmission at the expense of others. The ultimate reasons for their increased transmission are generally well understood. However, the molecular mechanisms driving their transmission above the Mendelian 50/50 ratio are poorly understood, especially in the case of selective exclusion of entire haploid genomes. A prime example for genome exclusion is hybridogenesis: some F1 hybrid species clonally transmit one of their haploid genomes (the selfish one) by selectively eliminating the other (the so-called ‘host genome’) during gamete formation. Here, I propose to use Bacillus stick insects to elucidate the molecular innovations that enable genome exclusion and lead to the evolution of hybridogenesis in Bacillus. The Bacillus system is uniquely suited for the proposed research as it is possible to introgress genome-eliminating elements into the genetic background of a ‘normal’ sexual species. This enables identification of genomic regions associated with genome exclusion by targeted genotyping. The project will answer three key questions: I) Bacillus comprises at least two hybridogenetic species that use different host genomes: how did host genome exclusion originate (independent origin vs host switch)? II) what is the genomic basis of genome exclusion?, and III) are cytoplasmic (maternally derived) components involved in genome exclusion? The methodological repertoire will comprise haplome phasing and phylogenomics using long-read data, experimental introgression and genetic mapping, and an experimental cytoplasm switch. By combining the methodology of different disciplines we will generate a cohesive understanding of the mechanistic basis of genome exclusion in a new model organism. The project addresses general hypotheses and will serve as a blueprint for genome exclusion studies with applicative potential in medicine and agriculture.
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