An effector of a necrotrophic fungal pathogen targets the calcium-sensing receptor in chloroplasts to inhibit host resistance.,Molecular Plant Pathology

当前位置： X-MOL 学术 › Mol. Plant Pathol. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

An effector of a necrotrophic fungal pathogen targets the calcium-sensing receptor in chloroplasts to inhibit host resistance.
Molecular Plant Pathology ( IF 4.8 ) Pub Date : 2020-02-27 , DOI: 10.1111/mpp.12922
Liguang Tang _{1,

2} , Guogen Yang ₃ , Ming Ma _{1,

2} , Xiaofan Liu _{1,

2} , Bo Li _{1,

2} , Jiatao Xie _{1,

2} , Yanping Fu ₂ , Tao Chen ₂ , Yang Yu ₄ , Weidong Chen ₅ , Daohong Jiang _{1,

2} , Jiasen Cheng _{1,

2}

Affiliation

SsITL, a secretory protein of the necrotrophic phytopathogen Sclerotinia sclerotiorum, was previously reported to suppress host immunity at the early stages of infection. However, the molecular mechanism that SsITL uses to inhibit plant defence against S. sclerotiorum has not yet been elucidated. Here, we report that SsITL interacted with a chloroplast‐localized calcium‐sensing receptor, CAS, in chloroplasts. We found that CAS is a positive regulator of the salicylic acid signalling pathway in plant immunity to S. sclerotiorum and CAS‐mediated resistance against S. sclerotiorum depends on Ca²⁺ signalling. Furthermore, we showed that SsITL could interfere with the plant salicylic acid (SA) signalling pathway and SsITL‐expressing transgenic plants were more susceptible to S. sclerotiorum. However, truncated SsITLs (SsITL‐NT1 or SsITL‐CT1) that lost the ability to interact with CAS do not affect plant resistance to S. sclerotiorum. Taken together, our findings reveal that SsITL inhibits SA accumulation during the early stage of infection by interacting with CAS and then facilitating the infection by S. sclerotiorum.

中文翻译：

坏死性真菌病原体的效应物靶向叶绿体中的钙敏感受体，以抑制宿主抗性。

SsITL是一种坏死性植物病原菌核盘菌的分泌蛋白，以前曾报道在感染的早期抑制宿主免疫力。然而，尚未阐明SsITL用于抑制植物抵抗核盘菌的分子机制。在这里，我们报道SsITL与叶绿体中的叶绿体定位钙敏感受体CAS相互作用。我们发现CAS是水杨酸信号转导途径在植物对S. sclerotiorum免疫中的正调节剂，而CAS介导的对S. sclerotiorum的抗性取决于Ca ²⁺发信号。此外，我们表明SsITL可能会干扰植物水杨酸（SA）信号传导途径，并且表达SsITL的转基因植物更容易感染核盘菌。但是，丧失了与CAS相互作用能力的截短的SsITL（SsITL-NT1或SsITL-CT1）不会影响植物对核盘菌的抗性。总之，我们的调查结果显示，在通过与中科院进行交互，然后促进感染感染的早期阶段SsITL抑制SA积累菌核病。

更新日期：2020-02-27

点击分享查看原文

点击收藏

公开下载

阅读更多本刊最新论文本刊介绍/投稿指南11