State Key Laboratory for Crop Stress Resistance and High-Efficiency Production and College of Plant Protection, Northwest A&F University, Yangling, 712100, Shaanxi, China.
State Key Laboratory for Crop Stress Resistance and High-Efficiency Production and College of Life Sciences, Northwest A&F University, Yangling, 712100, Shaanxi, China.
New Phytol. 2024 Dec;244(5):1961-1978. doi: 10.1111/nph.20146. Epub 2024 Sep 22.
Mitochondria-induced cell death is closely correlated with plant immune responses against pathogens. However, the molecular mechanisms by which pathogens manipulate mitochondria to suppress host resistance remain poorly understood. In this study, a haustorium-specific effector Pst11215 from the wheat stripe rust pathogen Puccinia striiformis f. sp. tritici (Pst) was characterized by host-induced gene silencing. The interaction partners regulated by Pst11215 were screened using the yeast two-hybrid system. In addition, Pst11215-mediated immune regulation modes were further determined. The results showed that Pst11215 was required for Pst virulence. Pst11215 interacted with the wheat voltage-dependent anion channel TaVDAC1, the negative regulator of wheat resistance to stripe rust, in mitochondria. Furthermore, the E3 ubiquitin ligase TaVDIP1 targeted and ubiquitinated TaVDAC1, which can be promoted by Pst11215. TaVDIP1 conferred enhanced wheat susceptibility to Pst by cooperating with TaVDAC1. Overexpression of TaVDIP1 reduced reactive oxygen species (ROS) accumulation and abnormal mitochondria. Our study revealed that Pst11215 functions as an important pathogenicity factor secreted to the host mitochondria to compromise wheat resistance to Pst possibly by facilitating TaVDIP1-mediated ubiquitination of TaVDAC1, thereby protecting mitochondria from ROS-induced impairment. This research unveils a novel regulation mode of effectors hijacking host mitochondria to contribute to pathogen infection.
线粒体诱导的细胞死亡与植物对病原体的免疫反应密切相关。然而，病原体操纵线粒体来抑制宿主抗性的分子机制仍知之甚少。在这项研究中，小麦条锈病菌 Puccinia striiformis f. sp. tritici (Pst) 中的一个吸器特异性效应物 Pst11215 通过宿主诱导的基因沉默被表征。使用酵母双杂交系统筛选受 Pst11215 调节的互作伙伴。此外，还进一步确定了 Pst11215 介导的免疫调节模式。结果表明，Pst11215 是 Pst 毒力所必需的。Pst11215 在质体中与小麦电压依赖性阴离子通道 TaVDAC1 相互作用，TaVDAC1 是小麦对条锈病抗性的负调节因子。此外，E3 泛素连接酶 TaVDIP1 靶向并泛素化 TaVDAC1，这可以被 Pst11215 促进。TaVDIP1 通过与 TaVDAC1 合作赋予小麦对 Pst 的增强易感性。TaVDIP1 的过表达减少了活性氧 (ROS) 的积累和异常线粒体。我们的研究表明，Pst11215 作为一种重要的分泌到宿主质体中的致病性因子，通过促进 TaVDIP1 介导的 TaVDAC1 泛素化，从而保护质体免受 ROS 诱导的损伤，从而损害小麦对 Pst 的抗性。这项研究揭示了效应子劫持宿主线粒体促进病原体感染的一种新的调控模式。
