Li Yue, Qu Xiangru, Yang Wenjuan, Wu Qin, Wang Xiaodong, Jiang Qiantao, Ma Jian, Zhang Yazhou, Qi Pengfei, Chen Guoyue, Zheng Youliang, Wang Xiaojie, Wei Yuming, Xu Qiang
State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China, Chengdu, Sichuan, China.
Triticeae Research Institute, Sichuan Agricultural University, Chengdu, Sichuan, China.
Nat Commun. 2025 Mar 24;16(1):2864. doi: 10.1038/s41467-025-58277-5.
Phytopathogens such as Puccinia striiformis f. sp. tritici (Pst) induce pigment retention at pathogen infection sites. Although pigment retention is commonly observed in diverse pathosystems, its underlying physiological mechanism remains largely unclear. Herein, we identify and characterize a wheat leaf senescence gene, TaSGR1, which enhances resistance against Pst by promoting leaf senescence and HO accumulation while inhibiting photosynthesis. Knockout of TaSGR1 (STAYGREEN) in wheat increases pigment retention and plant susceptibility. Pst_TTP1 (TaTrx-Targeting Protein 1), a secreted rust fungal effector critical for Pst virulence, binds to the plastidial thioredoxin TaTrx (Thioredoxin), preventing its translocation into chloroplasts. Within the chloroplasts, TaTrx catalyzes the transformation of TaSGR1 oligomers into monomers. These TaSGR1 monomers accumulate in the chloroplasts, accelerating leaf senescence, HO accumulation, and cell death. The inhibition of this oligomer-to-monomer transformation, caused by the failure of TaTrx to enter the chloroplast due to Pst_TTP1, impairs plant resistance against Pst. Overall, our study reveals the suppression of redox signaling cascade that catalyzes the transformation of TaSGR1 oligomers into monomers within chloroplasts and the inhibition of leaf chlorosis by rust effectors as key mechanisms underlying disease susceptibility.
诸如条锈菌（Puccinia striiformis f. sp. tritici，Pst）等植物病原体可诱导病原体感染部位的色素保留。尽管色素保留在多种病理系统中普遍存在，但其潜在的生理机制仍不清楚。在此，我们鉴定并表征了一个小麦叶片衰老基因TaSGR1，它通过促进叶片衰老和HO积累同时抑制光合作用来增强对Pst的抗性。小麦中TaSGR1（保持绿色）的敲除增加了色素保留和植物易感性。Pst_TTP1（TaTrx靶向蛋白1）是一种对Pst毒力至关重要的分泌型锈菌效应蛋白，它与质体硫氧还蛋白TaTrx（硫氧还蛋白）结合，阻止其转运到叶绿体中。在叶绿体内，TaTrx催化TaSGR1寡聚体向单体的转化。这些TaSGR1单体在叶绿体中积累，加速叶片衰老、HO积累和细胞死亡。由于Pst_TTP1导致TaTrx无法进入叶绿体而对这种寡聚体向单体转化的抑制，损害了植物对Pst的抗性。总体而言，我们的研究揭示了催化TaSGR1寡聚体在叶绿体内向单体转化的氧化还原信号级联的抑制以及锈菌效应蛋白对叶片褪绿的抑制是疾病易感性的关键机制。
