Open Access

ARTICLE

Metabolic Responses of Wheat Spike Tissue Associated with Fusarium Infection in Genotypes Differing in Type II Resistance

Jurica Duvnjak¹, Daniel Kujundzic², Katarina Sunic Budimir¹, John C. D’Auria², Valentina Spanic^1,*

1 Department of Small Cereal Crops Breeding and Genetics, Agricultural Institute Osijek, Juzno Predgradje 17, Osijek, Croatia
2 Department of Molecular Genetics Leibniz, Institute of Plant Genetics and Crop Plant Research (IPK Gatersleben), Gatersleben Corrensstraße 3, Seeland, Germany

* Corresponding Author: Valentina Spanic. Email:

(This article belongs to the Special Issue: Advances in the Breeding of High-Yielding and High-Quality Seeds)

Phyton-International Journal of Experimental Botany 2026, 95(7), 12 https://doi.org/10.32604/phyton.2026.082576

Received 18 March 2026; Accepted 18 May 2026; Issue published 30 July 2026

Abstract

In this study, metabolomic profiling using gas chromatography–mass spectrometry (GC-MS) revealed clear distinctions between Fusarium-infected and control wheat spikes, as shown by the separate clustering of infected samples. Out of 222 detected features, eight were found to be significantly altered in infected spikes compared to controls, highlighting specific metabolic changes associated with the plant’s response to Fusarium head blight (FHB) stress. In response to Fusarium infection, wheat exhibited significant metabolic reprogramming, with both reductions and accumulations of key metabolites. A decrease in 3-methoxytyramine (28.9–85.3%), octylamine, malic acid, and homonojirimycin suggests their early involvement in defence-related pathways either through rapid turnover, utilization in stress-induced lipid remodelling, energy diversion, or conversion into downstream protective compounds. Conversely, the accumulation of metabolites such as cis-aconitic acid, N-hexanoyl homoserine lactone, ribonic acid, and 1,3-diaminopropane points to disrupted central metabolism, increased microbial signalling activity, oxidative sugar degradation, and heightened polyamine catabolism. Together, these shifts reflect a coordinated host response involving energy redistribution, signalling modulation, and metabolic adjustments aimed at limiting pathogen spread and damage. Collectively, these findings provide insights into the metabolic responses associated with Fusarium infection in wheat genotypes that differ in type II resistance. Also, these results characterize metabolic responses to Fusarium infection in wheat genotypes differing in Type II resistance, used as a phenotypic reference of disease spread.

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Keywords

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