Matsui Hidenori, Nomura Yuko, Egusa Mayumi, Hamada Takahiro, Hyon Gang-Su, Kaminaka Hironori, Watanabe Yuichiro, Ueda Takashi, Trujillo Marco, Shirasu Ken, Nakagami Hirofumi
RIKEN Center for Sustainable Resource Science, Yokohama, Japan.
Graduate School of Environmental and Life Science, Okayama University, Okayama, Japan.
PLoS Genet. 2017 Oct 26;13(10):e1007037. doi: 10.1371/journal.pgen.1007037. eCollection 2017 Oct.
The induction of rapid cell death is an effective strategy for plants to restrict biotrophic and hemi-biotrophic pathogens at the infection site. However, activation of cell death comes at a high cost, as dead cells will no longer be available for defense responses nor general metabolic processes. In addition, necrotrophic pathogens that thrive on dead tissue, take advantage of cell death-triggering mechanisms. Mechanisms by which plants solve this conundrum remain described. Here, we identify PLANT SMY2-TYPE ILE-GYF DOMAIN-CONTAINING PROTEIN 1 (PSIG1) and show that PSIG1 helps to restrict cell death induction during pathogen infection. Inactivation of PSIG1 does not result in spontaneous lesions, and enhanced cell death in psig1 mutants is independent of salicylic acid (SA) biosynthesis or reactive oxygen species (ROS) production. Moreover, PSIG1 interacts with SMG7, which plays a role in nonsense-mediated RNA decay (NMD), and the smg7-4 mutant allele mimics the cell death phenotype of the psig1 mutants. Intriguingly, the psig1 mutants display enhanced susceptibility to the hemi-biotrophic bacterial pathogen. These findings point to the existence and importance of the SA- and ROS-independent cell death constraining mechanism as a part of the plant immune system.
诱导细胞快速死亡是植物在感染部位限制活体营养型和半活体营养型病原体的有效策略。然而，细胞死亡的激活代价高昂，因为死细胞将不再可用于防御反应或一般代谢过程。此外，在死组织上茁壮成长的坏死营养型病原体利用细胞死亡触发机制。植物解决这一难题的机制尚待描述。在这里，我们鉴定了植物SMY2型含异亮氨酸-GYF结构域蛋白1（PSIG1），并表明PSIG1有助于限制病原体感染期间的细胞死亡诱导。PSIG1失活不会导致自发损伤，并且psig1突变体中增强的细胞死亡与水杨酸（SA）生物合成或活性氧（ROS）产生无关。此外，PSIG1与在无义介导的RNA衰变（NMD）中起作用的SMG7相互作用，并且smg7-4突变等位基因模拟了psig1突变体的细胞死亡表型。有趣的是，psig1突变体对半活体营养型细菌病原体表现出增强的易感性。这些发现表明，作为植物免疫系统的一部分，SA和ROS非依赖性细胞死亡限制机制的存在及其重要性。
