Abstract
Wheat stem rust disease caused by Puccinia graminis f. sp. tritici (Pgt) is a global threat to wheat production. Fast evolving populations of Pgt limit the efficacy of plant genetic resistance and constrain disease management strategies. Understanding molecular mechanisms that lead to rust infection and disease susceptibility could deliver novel strategies to deploy crop resistance through genetic loss of disease susceptibility. We used comparative transcriptome-based and orthology-guided approaches to characterize gene expression changes associated with Pgt infection in susceptible and resistant Triticum aestivum genotypes as well as the non-host Brachypodium distachyon. We targeted our analysis to genes with differential expression in T. aestivum and genes suppressed or not affected in B. distachyon and report several processes potentially linked to susceptibility to Pgt, such as cell death suppression and impairment of photosynthesis. We complemented our approach with a gene co-expression network analysis to identify wheat targets to deliver resistance to Pgt through removal or modification of putative susceptibility genes.
Highlights
Stem rust caused by Puccinia graminis f. sp. tritici (Pgt) is one of the most devastating foliar diseases of wheat (Triticum aestivum) and barley (Hordeum vulgare)
Susceptibility was manifested by formation of large sporulating pustules in W2691+Sr9b networks are larger (W2691), while small pustules surrounded by a chlorotic halo were characteristic of Sr9b mediated-resistance at 6 days post-inoculation
Susceptibility differences between W2691 and W2691+Sr9b were evident at 6 dpi as formation of fungal colonies was present in both genotypes, but colony sizes were larger in W2691 than W2691+Sr9b (Figure 1)
Summary
Stem rust caused by Puccinia graminis f. sp. tritici (Pgt) is one of the most devastating foliar diseases of wheat (Triticum aestivum) and barley (Hordeum vulgare). As the fungus reaches the mesophyll cavity of the plant, it develops infection hyphae which penetrate plant cell walls and differentiate into specialized feeding structures, known as haustoria. Similar to other plant pathogens, cereal rust infections involve the translocation of effectors to the plant cell as a mechanism to shut down basal defenses activated by PAMP triggered immunity (PTI) and manipulate host metabolism (Dodds and Rathjen, 2010; Couto and Zipfel, 2016). The plant targets of effectors and other plant genes that mediate compatibility and facilitate pathogen infection are often regarded as susceptibility (S) genes (Lapin and van den Ackerveken, 2013; van Schie and Takken, 2014; Lo Presti et al, 2015)
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