Abstract
Phytophthora infestans, the causal agent of late blight disease, affects potatoes and tomatoes worldwide. This plant pathogen has a hemibiotrophic lifestyle, having an initial biotrophic infection phase during which the pathogen spreads within the host tissue, followed by a necrotrophic phase in which host cell death is induced. Although increasing information is available on the molecular mechanisms, underlying the distinct phases of the hemibiotrophic lifestyle, studies that consider the entire metabolic processes in the pathogen while undergoing the biotrophic, transition to necrotrophic, and necrotrophic phases have not been conducted. In this study, the genome-scale metabolic reconstruction of P. infestans was achieved. Subsequently, transcriptional data (microarrays, RNA-seq) was integrated into the metabolic reconstruction to obtain context-specific (metabolic) models (CSMs) of the infection process, using constraint-based reconstruction and analysis. The goal was to identify specific metabolic markers for distinct stages of the pathogen's life cycle. Results indicate that the overall metabolism show significant changes during infection. The most significant changes in metabolism were observed at the latest time points of infection. Metabolic activity associated with purine, pyrimidine, fatty acid, fructose and mannose, arginine, glycine, serine, and threonine amino acids appeared to be the most important metabolisms of the pathogen during the course of the infection, showing high number of reactions associated with them and expression switches at important stages of the life cycle. This study provides a framework for future throughput studies of the metabolic changes during the hemibiotrophic life cycle of this important plant pathogen.
Highlights
Late blight has been a major threat to global food security ever since the Irish potato famine of the mid-nineteenth century (Fry, 2008)
The final reconstruction of P. infestans accounted for 1,530 metabolites participating in 1,571 reactions (Table 2) belonging to 1,094 pathways (Table S2) and associated to 1,375 genes; 194 reactions are orphan
The pathways with more reactions in the reconstruction of P. infestans were associated with glycerophospholipid metabolism, fructose and mannose metabolism, and glycine, serine, and threonine metabolism (Figure 2, Table S2)
Summary
Late blight has been a major threat to global food security ever since the Irish potato famine of the mid-nineteenth century (Fry, 2008). Lee and Rose (2010) proposed a hypothetical model of transition between biotrophy and necrotrophy where effectors play an important role; for example, SNE1 acts by suppressing programmed cell death in the host and halting the effects of necrosis inducing proteins (NIPs) (Kelley et al, 2010) until the necrotrophic phase is initiated. This “simultaneous accelerator and brake model” (Lee and Rose, 2010) strategy of infection could explain the onset of necrosis and provides clues for the regulation of pathogenesis as well as the organism’s lifestyle
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