No abstract

Summary A distinguishing feature of Septoria leaf blotch disease in wheat is the long symptomless growth of the fungus amongst host cells followed by a rapid transition to necrotrophic growth resulting in disease lesions. Global reprogramming of host transcription marks this switch to necrotrophic growth. However no information exists on the components that bring about host transcriptional reprogramming. Gene‐silencing, confocal‐imaging and protein–protein interaction assays where employed to identify a plant homeodomain (PHD) protein, TaR1 in wheat that plays a critical role during the transition from symptomless to necrotrophic growth of Septoria. TaR1‐silenced wheat show earlier symptom development upon Septoria infection but reduced fungal sporulation indicating that TaR1 is key for prolonging the symptomless phase and facilitating Septoria asexual reproduction. TaR1 is localized to the nucleus and binds to wheat Histone 3. Trimethylation of Histone 3 at lysine 4 (H3K4) and lysine 36 (H3K36) are found on open chromatin with actively transcribed genes, whereas methylation of H3K27 and H3K9 are associated with repressed loci. TaR1 specifically recognizes dimethylated and trimethylated H3K4 peptides suggesting that it regulates transcriptional activation at open chromatin. We conclude that TaR1 is an important component for the pathogen life cycle in wheat that promotes successful colonization by Septoria.

Mycosphaerella graminicola (Zymoseptoria tritici commonly known as Septoria), the causal agent of Septoria Leaf Blotch (STB), is considered one of the major threats to European wheat production. Previous studies have shown the importance of ubiquitination in plant defence against a multitude of pathogens. However the ubiquitination machinery in wheat is under studied, particularly E2 enzymes that have the ability to control the ubiquitination and thereby the fate of many different target proteins. In this study we identify an E2 enzyme, Triticum aestivum Ubiquitin conjugating enzyme 4 (TaU4) that functions in wheat defence against Septoria. We demonstrate TaU4 to be a bona fide E2 enzyme through an E2 charging assay. TaU4 localises in both the cytoplasm and nucleus, therefore potentially interacting with E3 ligases and substrate proteins in multiple compartments. Virus Induced Gene Silencing of TaU4 in wheat leaves resulted in delayed development of disease symptoms, reduced Septoria growth and reproduction. We conclude that TaU4 is a novel negative regulator of defence against Septoria.

Zymoseptoria tritici is the causal pathogen of Septoria tritici blotch (STB), one of the most threatening wheat foliar diseases across temperate regions, causing up to 40% yield loss if untreated with fungicide (Orton et al., 2011). Z. tritici classification as a hemibiotrophic or a necrotrophic fungus is still a matter of debate; its life cycle is characterized by a long symptomless biotrophic phase, followed by a switch to a necrotrophic phase. During the biotrophic phase the Z. tritici spores germinate on the surface of leaves and hyphae invade the apoplastic space through the stomata. During this phase the fungus survives biotrophically, supposedly undetected by the host.The length of this period is variable, probably depending on environmental conditions, host recognition, or the properties of the pathogen strain (Dean et al., 2012). This latency period ends with Z. tritici rapidly switching to its necrotrophic feeding stage, where symptoms start to appear on foliar tissue in the form of chlorotic lesions that display characteristics of programmed cell death (Keon et al., 2007). The