Fusaric acid as a central hub of virulence: Reprogramming host physiology during Fusarium infection.

Abstract

Fusarium spp. include major soilborne pathogens that cause vascular wilt diseases in diverse crops. Fusaric acid (FA) is a non-host-specific toxin produced by some Fusarium species and contributes to virulence in several, but not all, host-pathogen systems. Traditionally, FA has been regarded as a broad-spectrum phytotoxin. However, emerging evidence indicates that FA acts beyond direct cellular damage, promoting pathogen colonization through the systematic reprogramming of host physiological processes. Herein, we proposed a pathogenic model with three interacting layers: (i) perturbation of plasma membrane function and ion homeostasis, including effects on H+-ATPase activity and ion transport; (ii) amplification through reactive oxygen species (ROS), lipid peroxidation and mitochondrial and chloroplast dysfunction; and (iii) modulation of hormone-redox signalling and programmed cell death (PCD). The strength and sequence of these responses depend on FA concentration, exposure time, host genotype and pathosystem. FA biosynthesis is controlled primarily by the FUB gene cluster and by broader transcriptional, nutritional and stress-responsive networks, but the relationship between FA production and virulence is context dependent. This review integrates current evidence on FA biosynthesis, stage-associated functions during infection, and cellular toxicity. Building upon these mechanistic insights, we discuss emerging mitigation strategies, including microbial degradation, targeted inhibition of FA biosynthesis, enhancement of host resistance, and metal ion antagonism. Collectively, this work establishes a conceptual framework for understanding Fusarium pathogenesis and provides a foundation for developing sustainable strategies for disease management.