Functional genomic characterization of germination and early infection of wheat by the fungus Zymoseptoria tritici.

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Providing enough food for all people on the planet is a major issue facing humanity in the 21st Century. As the Earth's population tops six billion the need to increase production of staple crops e.g. rice, wheat, banana is real. As the population grows to an anticipated nine billion by 2030 that demand will be even higher. In the UK wheat is a major crop, with 12.1 million tonnes, valued at more than £1.5 billion, produced in 2013. However, fungal disease, in particular septoria tritici blotch (STB), caused by Zymoseptoria tritici, is a major constraint on production. In untreated trials an average 20% of yield is lost, and in some cases field losses of 50% have been reported. Control of this disease could contribute an extra 2.4 - 6 million tonnes to the UK wheat harvest, and if applied to the global wheat harvest in 2013 would have delivered an extra 140 million tonnes into the food supply. There is no doubt that STB is a serious and immediate threat to global food security, and new control measures are urgently required. To initiate STB infection spores of Z. tritici alight on a leaf surface and germinate, beginning the disease process. This is followed by polarized growth development and passage into the interior of the leaf, usually within 12 hours. In susceptible wheat cultivars two days post-infection (dpi) the fungus has produced lateral branching and by 6-8 dpi this has developed to circumscribe a large area beneath the point of entry. At this stage the fungus has not yet invaded wheat cells and little evident symptomology is seen on the plant. However, 8-10 dpi symptoms begin to appear, concomitant with development of an incipient asexual reproductive structure, death of plant cells and a switch to parasitic growth. Around 14-21 dpi mature asexual spores are released, and the process starts again. This results in epidemic infections and is one reason why yield loss is so high. The hypothesis underpinning our planned research is that disruption of the very earliest events in infection e.g. Z. tritici spore germination, leaf penetration or initial hyphal development will prevent establishment of infection and initiation of disease. Thus targeting fungicide development to gene products essential for these developmental programs should deliver compounds that prevent disease and hence reduce yield loss. We have established a collaboration with Syngenta, a large Swiss based agribusiness to address our principle aim, which is to characterize the early events (0-4 dpi) in establishment of infection and initiation of disease by Z. tritici on wheat. Specifically we will: (1) Define the genes that are switched on by Z. tritici spores as they germinate on and initiate infection in the compatible wheat cultivar Avalon. This will provide a catalogue of genes that play a role in the initiation of disease, and that will be characterized in this project; (2) Characterize the cellular biology of both Z. tritici and wheat during early infection, and thus link specific genes to defined infection stages; (3) Undertake a combined bioinformatics and modelling assessment to prioritize Z. tritici genes involved in early infection for further analysis. This will allow us to select one hundred genes for analysis and (4) we will determine where the proteins encoded by the 100 genes are located within the fungus during infection. We will then inactivate each in turn and determine if this blocks infection, and if so at what stage? If lack of a protein results in the inability to cause infection then this protein has potential as a target for fungicide development.Taken together these experiments will not only reveal substantial new biology they will also identify proteins that can be utilized for rational target selection within the context of fungicide discovery.