Interactions and co-evolution of plants and pathogens

Abstract

Plant disease is one of the major factors threatening global food security. To understand why all plants aren’t immune to all diseases could help to develop new strategies to improve plant disease resistance. Although plants are constantly exposed to different pathogens, most plants are resistant to most pathogens and disease is exceptional. The disease outcome is determined by a triangle composed of host, pathogen and environment. Under a favored environmental condition, pathogens must access the plant interior by penetrating two physical barriers, the cuticle and the cell wall, and breaching antimicrobial compounds produced by plants. The few pathogens entered into plant tissues or cells have to face the sophisticated innate immune system of plants. Plant innate immune system have two-tiers, namely pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). PTI is initiated by recognition of pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) by plant cell surface pattern recognition receptors (PRRs). The first one named pattern- triggered immunity (PTI) which can halt most pathogen infections. However, different plant species possess distinct PRRs for PAMPs or DAMPs. Neither PRRs nor PAMPs are invariant, which may partially explain why all plants aren’t immune to all pathogens. Adapted pathogens evolved effectors which are delivered into plant cell to enhance pathogen virulence by suppressing PTI. In turn, plants have evolved resistance proteins (R proteins) to directly or indirectly recognize the pathogenic effectors. Most of the R proteins belong to the nucleotide binding-leucine rich repeat (NB-LRR) type intracellular receptors. The defense mediated by R proteins is called effector-triggered immunity (ETI). ETI activates stronger defense responses than PTI, usually results in hypersensitive cell death responses (HR) at infection sites. Effectors are extremely diverse and are indispensable to pathogens. Only in the presence of a cognate R effector association, ETI immunity can be activated. Therefore, ETI defense is species, race, or strain specific. In early 20th century, genetic analyses by Flor have revealed that disease resistance is controlled by corresponding pairs of effector and R genes. The so-called “gene-for-gene” hypothesis can largely explain why plants cannot immune to all pathogens. Both virulence of a pathogen and resistance of a plant are constantly changing and mount selective pressures on each other. The evolutionarily dynamic plant-pathogen interactions were well illustrated by a four phased “zig-zag” model. This coevolution generates stable polymorphisms, which result in genetic diversity in either pathogen virulent genes or plant resistance genes. The resistance of plants to pathogens exhibits polymorphic. Even our understanding about plant-pathogen interaction has progressed significantly in the past decade, but is still far from completely understood, and we are not able to control plant disease absolutely. Intensive future research is needed to help human being to win the Red Queen’s race with plant pathogens. Newly developed microbiota and genome editing tools will help us to fulfill the task.