Understanding the mechanism of chloroplast immunity.

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One of the "big challenges" for our next generation is to ensure global food security. This can be achieved through a combination of increasing productivity and selecting for plants which respond robustly to changing environmental conditions. Increasing productivity is challenging without bespoke local breeding solutions and this is reflected in the ever decreasing average annual crop yields achieved through conventional breeding. Crop losses due to biotic stress contribute disproportionately to yield losses, often around one quarter but in extreme cases in excess of three quarters of a crop. Thus developing novel approaches to restricting pathogen infections of crops and consequently yields must be a primary objective if we are to realistically ensure we can feed the estimated 9 billion people by 2050. We have recently shown that the chloroplast is a key battlefield in determining the eventual outcome of plant-microbe interactions. Aside from its ability to fix carbon, chloroplasts play a central role in integrating multiple environmental stimuli and sensing the metabolic status of the plant. As a principal source of reactive oxygen species, the site of a significant amount of primary carbon metabolism and synthesis of the majority of hormone metabolic precursors, the chloroplast represents a prime target for pathogen manipulation. Our pioneering work has shown that the chloroplast responds to recognition of conserved pathogen motifs (non-self) by generating a burst of reactive oxygen species (ROS) that we believe act as a defensive signal. It is not surprising therefore that successful pathogens deliver proteins and small molecules known as effectors - to intervene in this process. Our data indicate that pathogens, both bacterial and fungal, achieve this by reconfiguring expression of nuclear encoded plant genes and some effectors actually even enter the chloroplast. These effectors stop the ROS burst by suppressing photosynthesis - arguably one of the most important reactions on this planet - but we don't know how. What we do know is that effectors increase the production of a hormone called abscisic acid (ABA), and stopping ABA production makes the plant more resistant. Conversely, adding ABA stops the chloroplast ROS burst, enabling pathogen growth. Here our primary objective is to understand how recognition of non-self activates chloroplast immunity and how pathogen effector proteins have evolved to suppress this immunity. One major objective is to undertake detailed studies of the biophysical changes in the chloroplast during treatments that cause disease or induce defence. We will look at the changes in proteins within chloroplasts during these treatments and changes in the small molecules as well. Merging these data we will predict proteins that contribute to these processes. To access their role in defence we will change their abundance and looking at how those plants behave to pathogens. We will also work out how many effectors, and the functional nature of those effectors, enter the chloroplast. A second major strand of work is to visualise the dynamics of ROS production in the chloroplast and the nucleus during the transition from healthy to diseased plants. We are also interested in how organelles within the cell behave during disease and defence promoting challenges. To visualise this we have labelled different organelles in the cell with fluorescent markers and we will use these to monitor their behaviours during the infection process.As chloroplast immunity appears conserved, our longer term goal is to use the knowledge gained from these studies in novel re-engineering or intervention strategies that will provide plants with broad spectrum resistance against pathogens.