Phytophthora species are destructive plant pathogens that cause significant crop losses worldwide. To understand plant susceptibility to oomycete pathogens and to explore novel disease resistance strategies, we employed the Arabidopsis thaliana–Phytophthora parasitica model pathosystem and screened for A. thaliana T‐DNA insertion mutant lines resistant to P. parasitica. This led to the identification of the resistant mutant 267‐31, which carries two T‐DNA insertion sites in the promoter region of the ethylene‐responsive factor 19 gene (ERF019). Quantitative reverse transcription PCR (RT‐qPCR) assays showed that the expression of ERF019 was induced during P. parasitica infection in the wild type, which was suppressed in the 267‐31 mutant. Additional erf019 mutants were generated using CRISPR/Cas9 technology and were confirmed to have increased resistance to P. parasitica. In contrast, ERF019 overexpression lines were more susceptible. Transient overexpression assays in Nicotiana benthamiana showed that the nuclear localization of ERF019 is crucial for its susceptible function. RT‐qPCR analyses showed that the expression of marker genes for multiple defence pathways was significantly up‐regulated in the mutant compared with the wild type during infection. Flg22‐induced hydrogen peroxide accumulation and reactive oxygen species burst were impaired in ERF019 overexpression lines, and flg22‐induced MAPK activation was enhanced in erf019 mutants. Moreover, transient overexpression of ERF019 strongly suppressed INF‐triggered cell death in N. benthamiana. These results reveal the importance of ERF019 in mediating plant susceptibility to P. parasitica through suppression of pathogen‐associated molecular pattern‐triggered immunity.

中文翻译：

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拟南芥基因AtERF019通过抑制PAMP触发的免疫来负调节植物对寄生疫霉的抗性。

疫霉属植物是破坏性植物病原体，其在世界范围内造成严重的农作物损失。为了理解植物易感性卵菌病原体和探索新的抗病性策略，我们采用的拟南芥-寄生疫霉模型病害系统并筛选拟南芥T-DNA插入突变体品系抗性P.寄生。这导致鉴定出抗性突变体267-31，该突变体在乙烯反应因子19基因（ERF019）的启动子区域带有两个T-DNA插入位点。定量逆转录PCR（RT-qPCR）分析表明ERF019的表达在野生型寄生性疟原虫感染在267-31突变体中被抑制。其他erf019突变体是使用CRISPR / Cas9技术产生的，并被证实对寄生疟原虫具有增强的抗性。相反，ERF019过表达株更易感。本氏烟草的瞬时过表达测定表明，ERF019的核定位对其敏感功能至关重要。RT-qPCR分析表明，与野生型感染相比，突变体中多种防御途径的标记基因表达明显上调。Flg22诱导的过氧化氢积累和活性氧爆发在ERF019过表达品系中受损，而flg22诱导的MAPK活化在erf019突变体中得到增强。此外，ERF019的瞬时过表达强烈抑制了本氏烟草中由INF触发的细胞死亡。这些结果揭示了ERF019在介导植物对寄生性疟原虫的敏感性中的重要性。 通过抑制病原体相关的分子模式触发的免疫力。