EPIPAT · Unraveling the Epigenetic Arms Race Between Plants and Pathogens

Plant-pathogen interactions are complex processes involving molecular and physiological changes in both the host and the pathogen. An increasing number of reports are pointing towards the role of epigenetics in plant defense against pathogens. However, several gaps currently prevent us from fully understanding the extent of chromatin changes as well as their functions during infection. We recently showed that a bacterial virulence factor induces global changes in DNA methylation. My research group also discovered that genes encoding epigenetic factors typically expressed solely during the reproductive phase of the plant life cycle are induced by pathogen infection (abbreviated “RePat” genes). Surprisingly, mutations affecting RePat genes reduce infection suggesting that RePat genes enhance susceptibility to the pathogens. Here, I hypothesize that pathogens hijack the expression of RePat genes to counter-act the innate plant epigenetic defense. In EPIPAT, I will determine the precise spatial and temporal changes in epigenetic marks during infection. We will investigate how RePat genes are induced during infection as well as characterize their function in regulating the epigenome during infection. In EPIPAT, I aim to shed light on a neglected battlefield of host/pathogen interactions, the epigenetic arms race between plants and pathogens. EPIPAT will generate essential data and insights that will open the field's understanding of how epigenetic changes contribute to the plant's defense. The induction of reproduction-specific epigenetic factors during infection suggests that similar nuclear reprogramming mechanisms might be at play in both situations. Exploring their role during infection is bound to provide invaluable insights into their role during reproduction and help us establish evolutionary parallels between reproduction and defense.