ABSTRACT
Introduction Plants are generally immune to most pathogenic microbes due to their innate defense systems, but the exceptional combination of a susceptible host and a pathogen species (or race) can result in disease [1]. Plants have two types of defense mechanism against attack by pathogenic microbes: one against general microorganisms, and the other against specic pathogen races [2],[3]. e general defense mechanism is known as a pathogen-associated molecular pattern (PAMP) triggered immunity (PTI). PTI is initiated by extracellular surface receptors that recognize general features of microorganisms such as bacterial agellin [4],[5], chitosans (the deacetylated product of chitin [6]), and N-acetylchitooligosaccharides (the backbone fragment of the fungal cell wall [7]). As a result of coevolution, plant pathogens have developed various strategies to overcome PTI. One of them is an eector-triggered susceptibility (ETS), which deploys PTI-suppressing pathogen eectors [3]. Many eectors have been identied, and their functions and delivery systems are well studied in Gram-negative bacteria [8]. However, only a few eectors have been reported in plant pathogenic fungi, and their functions in PTI suppression and secretion mechanisms are still unknown [2],[3]. e more specic defense mechanism against pathogen ETS is known as eectortriggered immunity (ETI), which is stimulated by plant surveillance proteins (Rproteins) that specically recognize one of the pathogen’s eector proteins (Avr proteins). ETI is an accelerated and magnied defense response compared to PTI: in bacterial and fungal pathosystems, the same defense genes are related to both defense mechanisms, but they display stronger and faster activation in ETI than in PTI [9],[10]. ETI is accompanied by the active cell death of infected cells, the hypersensitive response (HR), which is known as the ultimate defense mechanism of plants [11]. However, certain pathogens avoid ETI by altering a target eector to prevent the recognition of a particular surveillance protein and/or by deploying other eectors that directly suppress ETI [12],[13].
