Abstract
Rice blast caused by Magnaporthe oryzae is one of the most serious fungous diseases in rice. In the past decades, studies have reported that numerous M. oryzae effectors were secreted into plant cells to facilitate inoculation. Effectors target host proteins to assist the virulence of pathogens via the localization of specific organelles, such as the nucleus, endoplasmic reticulum, chloroplast, etc. However, studies on the pathogenesis of peroxisome-targeting effectors are still limited. In our previous study, we analyzed the subcellular localization of candidate effectors from M. oryzae using the agrobacterium-mediated transient expression system in tobacco and found that MoPtep1 (peroxisomes-targeted effector protein 1) localized in plant peroxisomes. Here, we proved that MoPtep1 was induced in the early stage of the M. oryzae infection and positively regulated the pathogenicity, while it did not affect the vegetative growth of mycelia. Subcellular localization results showed that MoPtep1 was localized in the plant peroxisomes with a signal peptide and a cupredoxin domain. Sequence analysis indicated that the homologous protein of MoPtep1 in plant-pathogenic fungi was evolutionarily conserved. Furthermore, MoPtep1 could suppress INF1-induced cell death in tobacco, and the targeting host proteins were identified using the Y2H system. Our results suggested that MoPtep1 is an important pathogenic effector in rice blast.
Highlights
IntroductionThe plant lives in an environment threatened by a variety of pathogens in nature; the plant has evolved to have a complete defense system to recognize pathogens and stimulate the immune response for pathogenic infection [1]
Publisher’s Note: MDPI stays neutralThe plant lives in an environment threatened by a variety of pathogens in nature; the plant has evolved to have a complete defense system to recognize pathogens and stimulate the immune response for pathogenic infection [1]
851 secreted protein genes were predicted based on RL-SAGE, MPSS, and SBS transcriptome results [17]
Summary
The plant lives in an environment threatened by a variety of pathogens in nature; the plant has evolved to have a complete defense system to recognize pathogens and stimulate the immune response for pathogenic infection [1]. Plant cell-surface pattern recognition receptors (PRRs) recognize pathogen-associated molecular patterns (PAMPs) or microbe-associated molecular patterns (MAMPs) to stimulate pattern-triggered immunity (PTI), whereas pathogens secret effectors into plant cells to regulate PTI immunity. To defend against effector-triggered infection, plants have evolved resistant proteins (R proteins) to recognize effectors secreted by pathogens and trigger the ETI (effector-triggered immunity) to inhibit pathogen infection [2]. Plants evolve corresponding R proteins to recognize effectors and enhance disease resistance. Recent studies showed that Pseudomonas syringae effector HopZ1a localized in the plasma membrane and was recognized by SZE1 and with regard to jurisdictional claims in published maps and institutional affiliations
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