EAGER Proposal: Bet hedging as a mechanism for pathogenic variation in the rice blast fungus

University Of Kentucky Research Foundation, Lexington KY

Investigators

Abstract

Many microbes cause serious diseases of plants, humans and other animals. Both plants and animals possess immune systems that serve to recognize the presence of foreign organisms, which then leads to the initiation of defense responses that prevent further spread of the invading microbe. Recognition usually occurs when the host senses foreign proteins that are either secreted by the microbe as it attempts to establish the pathogenic state, or which form part of the organism's "coat." Unfortunately, pathogens have developed mechanisms that subvert the host's defenses, allowing them to grow and cause disease. For example, it is well known that the fungus Magnaporthe oryzae, which causes a devastating disease of rice known as blast, can avoid recognition by the plant through the mutation or loss of genes that code for proteins that would normally bind to specific resistance receptors in the rice plant. Recent studies in the investigator's laboratory imply the existence of a novel mechanism by which rice blast, and probably other pathogenic microbes, may escape host recognition. The hypothesized mechanism involves a bet hedging strategy in which genetically identical fungal colonies vary the types of proteins they secrete, thereby evading recognition by the host immune system. This project seeks direct evidence that this mechanism is employed during an infection. Any given M. oryzae strain has the potential to secrete hundreds of proteins during the infection process, many of which could elicit a defense reaction. However, current data suggest that the fungus bet-hedges against recognition by expressing different secreted protein subsets in fungal colonies that are genetically identical to one another. Such clonal variation in gene expression is believed to be a risk-spreading strategy that increases the chance of infection success on unpredictable plant genotypes. The goal of this project is to test this hypothesis and thereby improve understanding of the recognition processes between pathogens and their hosts. The specific objectives of the planned research are to: 1) Use RNAseq of individual infection sites to test for variable expression of fungal genes whose products elicit resistance in rice; 2) Use differential RNAseq to establish a causal link between mesothetic host reactions and the variable expression of one or more fungal avirulence genes. The central hypothesis is transformative because it establishes a new paradigm for plant-microbe recognition, with the potential to revolutionize current thinking in the field. The knowledge generated in the project could alter how plants are bred for disease resistance and may lead to novel therapeutic strategies for microbial diseases of human and other animals. The project will provide research training for an existing graduate student, who will also attend a Next Generation Sequencing and Bioinformatics workshop during the term of the project. These training opportunities will greatly expand her skill set and thereby enhance future career prospects.