International Symposium on Cereal Leaf Blights 2019 | University College Dublin, Ireland | 22-24 May 2019

Epigenetic control of effector genes in the wheat pathogen Zymoseptoria tritici

Lukas Meile
ETH Zurich

Julien Alassimone
ETH Zurich

Parvathy Krishnan
University of Copenhagen

Andrea Sánchez-Vallet*
ETH Zurich

Oral Presentation
Host-Pathogen Interactions

Moore Auditorium, UCD O'Brien centre for Science
23 May 2019, 12:00

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Fungal plant pathogens have a large repertoire of genes encoding putative effectors, which are presumed to aid infection. A large fraction of these genes is expressed only at low levels during in vitro growth but concertedly upregulated at specific stages of the infection. This tight regulation in time and space is postulated to avoid negative effects associated with mis-expression of effector genes, such as recognition by the host, autotoxicity or misuse of resources. Like in other fungal plant pathogens, many putative effector genes of Zymoseptoria tritici are located in transposable element-rich regions of the genome. These regions are usually heterochromatic and the expression of effector genes residing therein has therefore been hypothesized to be controlled by epigenetic mechanisms. In this work, we aim to determine the role of epigenetics in effector gene regulation in Z. tritici. We used reporter genes to monitor transcriptional activity at specific effector loci and showed that several effector genes are silenced in the absence of the host. During host colonization, de-silencing of effector genes occurs mostly when the fungus enters the host. Both increasing the levels of histone acetylation and abolishing histone H3 lysine 27 methylation impaired silencing, indicating that chromatin de-condensation plays a crucial role for effector gene activation. This research will contribute to our understanding  on how the activity of the promoter and the genomic location enable fast induction of effector genes, while preventing the negative effects associated with mis-regulation of effector genes.