![]() This implies that the physiology of the host tissue changes throughout the infection cycle, and consequently, also the nutrients available for the pathogen ( 13). Typically, after 3 to 6 days, this biotrophic phase is followed by a necrotrophic phase during which the lesion becomes necrotic and new sporangia emerge ( 11, 12). Moreover, P. infestans is a hemibiotrophic pathogen that requires viable host cells during the initial stages of the infection cycle, the so-called biotrophic phase with minimal symptoms. Oomycetes are considered osmotrophs that extracellularly catabolize complex host polymers, such as proteins, sugars, and fatty acids, using an arsenal of secreted enzymes, followed by the import of degraded nutrients into the cell ( 10). Both the apoplastic hyphae and haustoria provide close contact with the plant, facilitating the exchange of effectors and nutrients ( 9). From there, P. infestans colonizes the mesophyll hyphae grow in the apoplast while forming intracellular feeding structures called haustoria. These encyst and germinate to form a germ tube with an appressorium to penetrate epidermal cells of the plant. P. infestans sporangia are aerially dispersed, and after landing on a plant surface, these can release flagellate zoospores ( 8). Hence, there is a continuous quest for novel more durable control strategies. The pathogen has a highly flexible genome facilitating rapid adaptation to control strategies, be it resistant cultivars or chemical agents ( 6), and its profuse sporulation causes P. infestans to spread extremely fast ( 7). The most well-known oomycete is Phytophthora infestans, the causal agent of late blight disease on tomato and potato, which leads to significant yield losses worldwide ( 5). These share morphological characteristics with fungi, yet belong to the Stramenopiles, a eukaryotic lineage that besides oomycetes also includes diatoms and brown algae ( 4). A class of organisms comprising important plant and animal pathogens is the oomycetes ( 3). While increasing knowledge has been gained on secreted effector proteins that facilitate host colonization ( 2), the nature of pathogen nutrition remains underexplored. Plants and pathogens maintain a complex relationship that generally involves the secretion of effector proteins by the pathogen to manipulate plant cell processes and the scavenging of nutrients from the host by the pathogen to support its growth and proliferation ( 1). ![]() This integrated metabolic model for the P. infestans-tomato interaction provides a framework to integrate data and generate hypotheses about in planta nutrition of P. infestans throughout its infection cycle. As infection progresses, P. infestans performs less de novo synthesis of metabolites and scavenges more metabolites from tomato. This revealed profound changes in pathogen-host metabolism during infection. ![]() We also exploited dual-transcriptome data of a time course of a full late blight infection cycle on tomato leaves and integrated the expression of metabolic enzymes in the model. This showed, for example, that P. infestans, a thiamine auxotroph, depends on certain metabolic reactions of the tomato thiamine biosynthesis. We used this integrated model to simulate metabolic fluxes from host to pathogen and explored the topology of the model to study the dependencies of the metabolism of P. infestans on that of tomato. Here, we reconstructed an integrated metabolic model of P. infestans and tomato ( Solanum lycopersicum) by integrating two previously published models for both species. To date, the nutrient flux from host to pathogen during infection has hardly been studied, and the interlinked metabolisms of the pathogen and host remain poorly understood. P. infestans is a hemibiotrophic pathogen, and during infection, it scavenges nutrients from living host cells for its own proliferation. The oomycete pathogen Phytophthora infestans causes potato and tomato late blight, a disease that is a serious threat to agriculture.
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