Investigating control of Ustilago maydis teliospore formation, dormancy and germination

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Crop production is a major component of the multi-billion dollar agricultural and agrifood sector that employs over two million Canadians. This production is threatened by an increase in fungal diseases that are spread by massive numbers of resistant spores. The current research focus on disease formation has not produced new ways to fight fungal diseases. Here I present an alternative focus, blocking spore production and disease spread, as an area where novel approaches for battling fungi could be developed. We have known about the role of spores since the discovery that microbes cause disease. Obvious signs of fungal disease in crops are often associated with spore production. However our knowledge of how fungi influence plants to help them develop and disperse spores is limited. My laboratory has developed techniques for investigating fungal plant disease using the common corn smut fungus, Ustilago maydis. We are determining: 1. How the fungus uses hormones to time spore formation; 2. How different fungi manipulate the host to produce spores, and 3. How dormant spores become active We discovered that U. maydis produces cytokinins (CKs), plant hormones that alter the plant as disease develops. U. maydis can also detect CKs during infection suggesting that it might monitor levels of CKs in order to time the production of its spores. We will investigate which genes the fungus and the plant turn on and off when CKs are present. Then we will determine how altering the expression of these genes influences spore development. We found that U. maydis can cross with a closely related fungus Sporisorium reilianum to produce hybrids. Both parents infect maize but U. maydis produces disease symptoms and spores around the site of infection, whereas, S. reilianum enters maize and grows systemically producing disease symptoms and spores only in the tassels and cobs. The hybrids grow similar to U. maydis in culture but in the plant they do not produce spores. We will determine which of the U. maydis pathogenesis genes are turned on or off in the hybrid during infection and whether changing the expression of certain genes can help the hybrid form spores. This will identify genes with roles in spore production and uncover how hybridization could lead to new types of pathogens. In the third project we will investigate another aspect of disease spread, the germination of spores. When formed, these resistant structures become dormant. We have developed tools to help us study how U. maydis controls the return to metabolic activity as spores germinate. Understanding this return to a disease producing state is controlled may allow us to uncover novel ways of stopping it and of preventing disease spread. The knowledge gained through this research will contribute to the development of novel approaches for preventing fungal disease spread to improve the sustainability of crop production