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Impact of Horizontal Mini-Chromosome Transfer on the Function and Evolution of a Major Cereal Pathogen

Subject Area Plant Breeding and Plant Pathology
General Genetics and Functional Genome Biology
Evolution and Systematics of Plants and Fungi
Microbial Ecology and Applied Microbiology
Organismic Interactions, Chemical Ecology and Microbiomes of Plant Systems
Term since 2025
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 562695474
 
Fungal plant pathogens are a major threat to global food security, causing 10–23% of annual crop losses. Developing resistant crops is challenging due to the rapid pathogen evolution, often rendering control measures ineffective. My recent work showed that horizontal gene flow fuels genome evolution in clonal lineages of a major plant-pathogenic fungus, enhancing their resistance to control efforts. Horizontal gene flow has been recognized as crucial in fungal evolution, allowing clonal pathogens, often responsible for disease pandemics, to overcome genetic constraints and maintain their pathogenicity even in the absence of sexual recombination. I established that accessory mini-chromosomes (mChrs) act as vehicles for horizontal gene transfer in fungi. In Magnaporthe oryzae, a devastating cereal pathogen, I demonstrated that horizontal transfer of mChrs occurs in agricultural fields. Specifically, a mChr called mChrA was repeatedly horizontally transferred from sexual lineages infecting wild grasses to clonal lineages infecting crops, driving genome evolution in clonal populations. However, the functional role of mChrA in key biological processes, such as mating and disease, as well as the mechanisms facilitating its recurrent horizontal transfer, and the selection pressures maintaining it in agricultural populations, remain unknown. These gaps in knowledge present an opportunity to advance our understanding of pathogen evolution. My preliminary findings suggest that mChrA impairs sexual spore formation, alters disease dynamics, and may be recurrently transferred due to its chromatin structure. Additionally, its intermediate frequencies in agricultural field populations may reflect a trade-off between the advantages and drawbacks of harboring mChrA, possibly driven by its selfish genetic nature. I hypothesize that mChrA promotes clonality, influences disease outcomes, and its horizontal transferability is enhanced due to its chromatin structure. Furthermore, I hypothesize that mChrA experiences balancing selection pressures in agricultural populations, influenced by the selfish nature of mChrA, which helps sustain its presence and function. To test these hypotheses, I will pursue three objectives: 1. Determine the extent to which mChrA promotes clonality and identify the genes underlying this phenotype. 2. Establish mChrA’s impact on disease severity and host range, and identify causal genes. 3. Identify chromatin-related mechanisms facilitating mChrA transfer and the genes involved. By integrating fungal genetics, genomics, and plant pathology, I will establish the role of horizontal mChr transfer in facilitating the rapid evolution of plant pathogens and help explain their resilience to new plant hosts and control measures. This understanding will lay the groundwork for innovative biocontrol strategies, improving crop resilience and enhancing global food security.
DFG Programme Emmy Noether Independent Junior Research Groups
 
 

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