Abstract
Plants constantly suffer from simultaneous infection by multiple pathogens, which can be divided into biotrophic, hemibiotrophic, and necrotrophic pathogens, according to their lifestyles. Many studies have contributed to improving our knowledge of how plants can defend against pathogens, involving different layers of defense mechanisms. In this sense, the review discusses: (1) the functions of PAMP (pathogen-associated molecular pattern)-triggered immunity (PTI) and effector-triggered immunity (ETI), (2) evidence highlighting the functions of salicylic acid (SA) and jasmonic acid (JA)/ethylene (ET)-mediated signaling pathways downstream of PTI and ETI, and (3) other defense aspects, including many novel small molecules that are involved in defense and phenomena, including systemic acquired resistance (SAR) and priming. In particular, we mainly focus on SA and (JA)/ET-mediated signaling pathways. Interactions among them, including synergistic effects and antagonistic effects, are intensively explored. This might be critical to understanding dynamic disease regulation.
Highlights
Since they exposed to challenging environments, plants face great threats from pathogen infections.Pathogens can be classified into three categories—biotrophic, necrotrophic, and hemibiotrophic pathogens—according to their different infection strategies [1]
Glucosinolates are produced in the trichomes of Arabidopsis, and their biosynthesis is regulated by the basic helix–loop–helix
To overcome the virulence of effectors from pathogens, plants, in turn, establish effector-triggered immunity (ETI) by recognizing virulent effectors via corresponding receptor resistance (R) proteins in a specific gene-to-gene manner, which is commonly accompanied by a hypersensitive response in the form of rapid cell death, which limits the spread of the pathogen from infection sites
Summary
Since they exposed to challenging environments, plants face great threats from pathogen infections. Most of the necrotrophs infect a broad range of hosts, except for a few ones. The fungal pathogens Botrytis cinerea, Alternaria brassicicola, and Sclerotinia sclerotiorum are taken as general examples of necrotrophic infections that kill hosts using toxic metabolites, enzymes, or microRNAs [2,3,4]. We will summarize and explore recent findings on pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI) and effector-triggered immunity (ETI), especially the roles of the three classical hormone pathways: salicylic acid (SA) and jasmonic acid (JA)/ethylene (ET) pathways (Figures 1 and 2), as well as the cross-talk among them (Figure 3), and other defense mechanisms. The regulation by hormone pathways involved in small molecules-mediated defenses such as pipecolic acid, SAR, and priming are discussed. Most of what we discuss concerns research performed in Arabidopsis; examples from other species are introduced as well, where appropriate
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