Department of Entomology and Plant Pathology, University of Arkansas, Fayetteville, AR, 72703, USA.
Department of Agronomy, Horticulture and Plant Science, South Dakota State University, Brookings, SD, USA.
Sci Rep. 2022 Mar 30;12(1):5388. doi: 10.1038/s41598-022-09335-1.
The plant pathogenic bacterium Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) has become a paradigm to investigate plant-bacteria interactions due to its ability to cause disease in the model plant Arabidopsis thaliana. Pst DC3000 uses the type III secretion system to deliver type III secreted effectors (T3SEs) directly into the plant cytoplasm. Pst DC3000 T3SEs contribute to pathogenicity by suppressing plant defense responses and targeting plant's physiological processes. Although the complete repertoire of effectors encoded in the Pst DC3000 genome have been identified, the specific function for most of them remains to be elucidated. Among those effectors, the mitochondrial-localized T3E HopG1, suppresses plant defense responses and promotes the development of disease symptoms. Here, we show that HopG1 triggers necrotic cell death that enables the growth of adapted and non-adapted pathogens. We further showed that HopG1 interacts with the plant immunity-related protein AtNHR2B and that AtNHR2B attenuates HopG1- virulence functions. These results highlight the importance of HopG1 as a multi-faceted protein and uncover its interplay with AtNHR2B.
植物病原细菌丁香假单胞菌 pv.番茄 DC3000（Pst DC3000）因其能够在模式植物拟南芥中引起疾病而成为研究植物-细菌相互作用的典范。Pst DC3000 使用 III 型分泌系统将 III 型分泌效应物（T3SE）直接输送到植物细胞质中。Pst DC3000 T3SE 通过抑制植物防御反应和靶向植物生理过程来促进致病性。尽管已经确定了 Pst DC3000 基因组中编码的完整效应物库，但它们的大多数特定功能仍有待阐明。在这些效应物中，定位于线粒体的 T3E HopG1 抑制植物防御反应并促进疾病症状的发展。在这里，我们表明 HopG1 触发坏死性细胞死亡，从而使适应和不适应的病原体得以生长。我们进一步表明，HopG1 与植物免疫相关蛋白 AtNHR2B 相互作用，并且 AtNHR2B 减弱了 HopG1 的毒力功能。这些结果强调了 HopG1 作为一种多方面蛋白的重要性，并揭示了其与 AtNHR2B 的相互作用。
