The arms race between tomato and Fusarium oxysporum

Abstract

The interaction between tomato and Fusarium oxysporum f. sp. lycopersici has become a model system for the study of the molecular basis of disease resistance and susceptibility. Gene-for-gene interactions in this system have provided the basis for the development of tomato cultivars resistant to Fusarium wilt disease. Over the last 6 years, new insights into the molecular basis of these gene-for-gene interactions have been obtained. Highlights are the identification of three avirulence genes in F. oxysporum f. sp. lycopersici and the development of a molecular switch model for I-2, a nucleotide-binding and leucine-rich repeat-type resistance protein which mediates the recognition of the Avr2 protein. We summarize these findings here and present possible scenarios for the ongoing molecular arms race between tomato and F. oxysporum f. sp. lycopersici in both nature and agriculture.

Figure 1

Working model depicting the molecular arms race between tomato and Fusarium oxysporum f. sp. lycopersici (Fol). (a) Non‐pathogenic F. oxysporum strains trigger the induction of basal defence preventing disease. This pathogen‐associated molecular pattern (PAMP)‐triggered immunity (PTI) is probably conferred by receptor‐like kinases (RLKs). (b) Effectors, such as Avr2, suppress the PTI response, allowing pathogenic Fol strains to cause disease. (c) Perception of Avr2 by the nucleotide‐binding and leucine‐rich repeat (NB‐LRR) protein I‐2 triggers a conformational change, allowing it to activate host defence. (d) Avr1‐carrying Fol strains frustrate I‐2‐mediated defence, resulting in disease development. (e) Avr1 is recognized by I or I‐1, resulting in the activation of host defences.