Identification and Functional Analysis of AopN, an Effector that Induces Programmed Cell Death in Plants.

Int J Mol Sci

State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing 100193, China.

Published: August 2020

AI Article Synopsis

  • Bacterial fruit blotch (BFB) is a serious disease affecting watermelons, causing major economic losses, but the mechanisms behind its pathogenicity are not fully understood.
  • Research has identified a new effector protein, AopN, which is found on the cell membrane of the bacteria and is shown to suppress plant immune responses by inhibiting reactive oxygen species bursts and triggering programmed cell death.
  • AopN also interacts with watermelon proteins ClHIPP and ClLTP, indicating its role in modulating plant immune responses and suggesting it may be crucial for the pathogen’s virulence.

Article Abstract

Bacterial fruit blotch (BFB), caused by , seriously affects watermelon and other cucurbit crops, resulting in significant economic losses. However, the pathogenicity mechanism of is not well understood. Plant pathogenic bacteria often suppress the plant immune response by secreting effector proteins. Thus, identifying effector proteins and determining their functions may improve our understanding of the underlying pathogenetic mechanisms. In this study, a novel effector, AopN, which is localized on the cell membrane of was identified. The functional analysis revealed that AopN significantly inhibited the flg22-induced reactive oxygen species burst. AopN induced a programmed cell death (PCD) response. Unlike its homologous protein, the ability of AopN to induce PCD was dependent on two motifs of unknown functions (including DUP4129 and Cpta_toxin), but was not dependent on LXXLL domain. More importantly, the virulence of the mutant of in significantly decreased, indicating that it was a core effector. Further analysis revealed that AopN interacted with watermelon ClHIPP and ClLTP, which responds to strain Aac5 infection at the transcription level. Collectively, these findings indicate that AopN suppresses plant immunity and activates the effector-triggered immunity pathway.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7504669PMC
http://dx.doi.org/10.3390/ijms21176050DOI Listing

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