Abstract
The Dothideomycete fungus Zymoseptoria tritici (previously known as Mycosphaerella graminicola and Septoria tritici) is the causative agent of Septoria tritici leaf blotch (STB) disease of wheat (Triticum aestivum L.). In Europe, STB is the most economically damaging disease of wheat, with an estimated ∼€1 billion per year in fungicide expenditure directed toward its control. Here, an overview of our current understanding of the molecular events that occur during Z. tritici infection of wheat leaves is presented. On the host side, this includes the contribution of (1) the pathogen-associated molecular pattern-triggered immunity (PTI) layer of plant defense, and (2) major Stb loci for resistance against Z. tritici. On the pathogen side of the interaction, we consolidate evidence from recent bioinformatic, transcriptomic and proteomic studies that begin to explain the contribution of Z. tritici effector proteins to the biphasic lifestyle of the fungus. This includes the discovery of chitin-binding proteins in the Z. tritici secretome, which contribute to evasion of immune surveillance by this pathogen, and the possible existence of ‘necrotrophic’ effectors from Z. tritici, which may actively stimulate host recognition in a manner similar to related necrotrophic fungal pathogens. We finish by speculating on how some of these recent fundamental discoveries might be harnessed to help improve resistance to STB in the world’s second largest food crop.
Highlights
The Dothideomycete fungus Zymoseptoria tritici is the causative agent of Septoria tritici leaf blotch (STB) disease of wheat (Triticum aestivum L.)
The asymptomatic phase typically lasts 7–10 days following inoculation depending on the particular cultivarisolate combination, after which there is a rapid transition to the symptomatic phase, which is frequently referred to as ‘necrotrophic.’ This second infection phase is typified by the large-scale reprogramming of both host and pathogen transcriptomes, a strong activation of host defense responses culminating in apoptotic-like rather than necrotic cell death and release of nutrients into the leaf apoplast and, as a consequence, a substantial build-up of fungal biomass (Keon et al, 2007; Yang et al, 2013b; Rudd et al, 2015)
Both Mg3LysM and Mg1LysM have a unique protective effect for Z. tritici, shielding the fungal cell wall from digestion by host chitinases (Marshall et al, 2011). This activity has not been observed for lysin motifs (LysM) effectors from other fungi including Ecp6. These results demonstrate the importance of chitin-binding effectors during the early stage of plant colonization
Summary
This includes the contribution of (1) the pathogen-associated molecular pattern-triggered immunity (PTI) layer of plant defense, and (2) major Stb loci for resistance against Z. tritici. On the pathogen side of the interaction, we consolidate evidence from recent bioinformatic, transcriptomic and proteomic studies that begin to explain the contribution of Z. tritici effector proteins to the biphasic lifestyle of the fungus. This includes the discovery of chitin-binding proteins in the Z. tritici secretome, which contribute to evasion of immune surveillance by this pathogen, and the possible existence of ‘necrotrophic’ effectors from Z. tritici, which may actively stimulate host recognition in a manner similar to related necrotrophic fungal pathogens.
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