The early response during the interaction of fungal phytopathogen and host plant

Abstract

Plants can be infected by a variety of pathogens, most of which can cause severe economic losses. The plants resist the invasion of pathogens via the innate or acquired immune system for surviving biotic stress. The associations between plants and pathogens are sophisticated beyond imaging and the interactions between them can occur at a very early stage after their touching each other. A number of researchers in the past decade have shown that many biochemical events appeared even as early as 5 min after their touching for plant disease resistance response. The early molecular interactions of plants and pathogens are likely to involve protein phosphorylation, ion fluxes, reactive oxygen species (ROS) and other signalling transduction. Here, we reviewed the recent progress in the study for molecular interaction response of fungal pathogens and host plant at the early infection stage, which included many economically important crop fungal pathogens such as cereal rust fungi, tomato Cladosporium fulvum, rice blast and so on. By dissecting the earlier infection stage of the diseases, the avirulent/virulent genes of pathogen or resistance genes of plant could be defined more clearly and accurately, which would undoubtedly facilitate fungal pathogenesis study and resistant crop breeding.

Keywords: avirulent genes; early infection; fungal pathogens; host plant; molecular interactions; resistance genes.

Figure 1.

A zigzag model of the plant immune system [28]. PTI: PAMP-triggered immunity; ETS: effector-triggered susceptibility; ETI: effector-triggered immunity; PAMPs: pathogen-associated molecular patterns; HR: hypersensitive cell death response. This model can be divided into four stages. In phase 1, plants recognize PAMPs via PRRs that triggered PTI. In phase 2, effectors of invading pathogens lead to ETS or interfere with PTI. In phase 3, an NB-LRR protein specifically recognizes a pathogen effector (indicated in red) directly or indirectly, resulting in ETI. The resistance or HR induced by ETI is faster and stronger than PTI. In phase 4, natural selection perhaps forms new effectors through horizontal gene flow (in blue) replacing the old effectors (in red), and plants generate new R genes to resist pathogens, resulting in ETI again.

Figure 2.

The flow chart of the interaction between stem rust fungus and barley. Barley with Rpg1 resistance gene inoculated with avirulent and viable stem rust fungal pathotype of Puccinia graminis f. sp. tritici MCCF triggered disease resistance responses. The RPG1 protein (in blue) constitutively expressed in host cells can be phosphorylated within 5 min by the interaction between Rpg1 gene product and RGD-binding protein and VPS9 protein (in red) in stem rust. The phosphorylation triggers a series of signalling pathways and the resistance mechanism in barley.