Liu Pengtao, Zhao Zhao, Tang Yaqi, Zhou Yangyang, Liu Jie, Xu Kaiqi, Chen Yaxin, Li Xiaoting, Tang Yaru, Yang Li
Frontiers Science Center for Molecular Design Breeding (MOE), State Key Laboratory of Agricultural and Forestry Biosecurity, MOA Key Lab of Pest Monitoring and Green Management, College of Plant Protection, China Agricultural University, Beijing 100193, China.
Frontiers Science Center for Molecular Design Breeding (MOE), State Key Laboratory of Agricultural and Forestry Biosecurity, MOA Key Lab of Pest Monitoring and Green Management, College of Plant Protection, China Agricultural University, Beijing 100193, China.
Cell Host Microbe. 2025 Sep 10;33(9):1606-1622.e10. doi: 10.1016/j.chom.2025.08.007. Epub 2025 Sep 2.
Light is essential for plant development, but its influence on pathogen virulence and immunity remains poorly understood. Here, we found that the Pseudomonas syringae DC3000 type III effector, AvrPtoB, exhibits virulence exclusively upon light exposure. This light-dependent regulation is controlled by the Arabidopsis transcription factor ELONGATED HYPOCOTYL 5 (HY5), a central regulator of photomorphogenesis. AvrPtoB targets HY5 in the nucleus, facilitating its ubiquitination and degradation. Genetic disruption of HY5 eliminates susceptibility to AvrPtoB and compromises plant immunity upon light exposure. HY5 enhances immunity by binding promoters of defense-related genes, activating their expression, and stabilizing the transcriptional coregulator NONEXPRESSOR OF PATHOGENESIS-RELATED (PR) GENES 1 (NPR1) by inhibiting its negative regulators NPR3/4. Both HY5-mediated immunity and light-dependent AvrPtoB virulence require NPR1. By contrast, during darkness, CONSTITUTIVELY PHOTOMORPHOGENIC 1 (COP1)-mediated HY5 degradation suppresses AvrPtoB virulence and HY5-enhanced immunity. These findings elucidate a mechanism in which light modulates bacterial virulence and plant immunity via an HY5-NPR1 module, advancing our understanding of light-pathogen-host interactions.
光对植物发育至关重要，但其对病原体毒力和免疫的影响仍知之甚少。在此，我们发现丁香假单胞菌DC3000的III型效应子AvrPtoB仅在光照下表现出毒力。这种光依赖性调控由拟南芥转录因子伸长下胚轴5（HY5）控制，HY5是光形态建成的核心调节因子。AvrPtoB在细胞核中靶向HY5，促进其泛素化和降解。HY5的基因破坏消除了对AvrPtoB的易感性，并损害了光照下的植物免疫。HY5通过结合防御相关基因的启动子、激活其表达以及通过抑制其负调节因子NPR3/4来稳定病程相关（PR）基因非表达子1（NPR1）来增强免疫。HY5介导的免疫和光依赖性AvrPtoB毒力都需要NPR1。相比之下，在黑暗中，组成型光形态建成1（COP1）介导的HY5降解抑制了AvrPtoB毒力和HY5增强的免疫。这些发现阐明了一种机制，即光通过HY5-NPR1模块调节细菌毒力和植物免疫，增进了我们对光-病原体-宿主相互作用的理解。
