Metabolomics and dual proteomics identify contrasting patterns of major pathways affected in asparagus shoot upon Fusarium infection

Witzel K; Djalali Farahani-Kofoet R; Döll S; Lindemann V; Cramer B; Humpf H; Zrenner R

Zusammenfassung

Aims: Infections with soil-borne pathogens have considerable detrimental effects on asparagus (Asparagus officinalis) growth and production, notably caused by the Fusarium species F. oxysporum f.sp. asparagi, F. proliferatum, and F. redolens. To get insight into the systemic effects of fungal infection on plant physiology to identify candidate resistance traits, we investigated this interaction using a multi omics approach. Methods: Asparagus plants were inoculated with one of the three Fusarium species. After 8 weeks, basal stem parts were harvested and subjected to metabolome and proteome analysis as well as detection of fungal DNA. Results: Upon infection, the pathogen spreads systemically from the root to the shoot and, consequently, fungal DNA and mycotoxins were detected in the basal part of the plant stem. Metabolite data revealed that the main pathway affected by Fusarium infections was “Fatty acids”, specifically the superclasses “Glycerophospholipids”, “Glycerolipids” and “Sphingolipids” being lower abundant upon infection. Another main pathway identified in the analysis was “Shikimates and Phenylpropanoids” with compounds assigned to these classes being mainly enriched upon infection. Proteome data revealed an induction of pathogen-defense proteins upon infection in asparagus, while proteins involved in vesicle trafficking and lipid metabolism were lower abundant. Conclusions: This indicates that not only lipid-based signaling processes are distorted by Fusarium, but also fundamental processes such as vesicle formation, membrane integrity and cell wall organization. In planta proteome analysis of F. oxysporum led to the identification of 1,488 fungal proteins, including proteins involved in metabolic and cellular processes as well as putative virulence factors. © The Author(s) 2024.