Zhang Chongyang, Fang Liang, He Feng, You Xiaoman, Wang Min, Zhao Tianxiao, Hou Yanyan, Xiao Ning, Li Aihong, Yang Jian, Ruan Jue, Francis Frédéric, Wang Guo-Liang, Wang Ruyi, Ning Yuese
State Key Laboratory for Biology of Plant Diseases and Insect Pests, Institute of Plant Protection, Chinese Academy of Agricultural Sciences, Beijing 100193, China.
Agricultural Genomics Institute at Shenzhen, Chinese Academy of Agricultural Sciences, Shenzhen 440307, China.
Sci Adv. 2025 Jan 3;11(1):eadr2441. doi: 10.1126/sciadv.adr2441.
The COP9 signalosome (CSN) is a highly conserved protein complex in eukaryotes, with CSN5 serving as its critical catalytic subunit. However, the role of CSN5 in plant immunity is largely unexplored. Here, we found that suppression of in rice enhances resistance against the fungal pathogen and the bacterial pathogen pv. () without affecting growth. OsCSN5 is ubiquitinated and degraded by the E3 ligase OsPUB45. Overexpression of increased resistance against and , while dysfunction of decreased resistance. In addition, OsCSN5 stabilized OsCUL3a to promote the degradation of a positive regulator OsNPR1. Overexpression of compromised accumulation of OsCUL3a, leading to stabilization of OsNPR1, whereas mutations in destabilized OsNPR1. These findings suggest that OsCSN5 stabilizes OsCUL3a to facilitate the degradation of OsNPR1, preventing its constitutive activation without infection. Conversely, OsPUB45 promotes the degradation of OsCSN5, contributing to immunity activation upon pathogen infection.
COP9信号体（CSN）是真核生物中一种高度保守的蛋白质复合物，CSN5作为其关键的催化亚基。然而，CSN5在植物免疫中的作用在很大程度上尚未被探索。在这里，我们发现水稻中OsCSN5的抑制增强了对真菌病原体稻瘟病菌和细菌病原体水稻白叶枯病菌（Xanthomonas oryzae pv. oryzae）的抗性，而不影响生长。OsCSN5被E3连接酶OsPUB45泛素化并降解。OsPUB45的过表达增加了对稻瘟病菌和水稻白叶枯病菌的抗性，而OsPUB45功能失调则降低了抗性。此外，OsCSN5稳定OsCUL3a以促进正向调节因子OsNPR1的降解。OsPUB45的过表达损害了OsCUL3a的积累，导致OsNPR1的稳定，而OsPUB45中的突变使OsNPR1不稳定。这些发现表明，OsCSN5稳定OsCUL3a以促进OsNPR1的降解，防止其在未感染时的组成型激活。相反，OsPUB45促进OsCSN5的降解，有助于病原体感染时的免疫激活。
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