Dogra Vivek, Duan Jianli, Lee Keun Pyo, Lv Shanshan, Liu Renyi, Kim Chanhong
Laboratory of Photosynthesis and Stress Signaling, Center for Excellence in Molecular Plant Sciences, Shanghai Center for Plant Stress Biology, Chinese Academy of SciencesShanghai, China.
Shanghai Center for Plant Stress Biology, Chinese Academy of SciencesShanghai, China.
Front Plant Sci. 2017 Jun 29;8:1145. doi: 10.3389/fpls.2017.01145. eCollection 2017.
Photosystem II reaction center (PSII RC) and light-harvesting complex inevitably generate highly reactive singlet oxygen (O) that can impose photo-oxidative damage, especially when the rate of generation exceeds the rate of detoxification. Besides being toxic, O has also been ascribed to trigger retrograde signaling, which leads to nuclear gene expression changes. Two distinctive molecular components appear to regulate O signaling: a volatile signaling molecule β-cyclocitral (β-CC) generated upon oxidation of β-carotene by O in PSII RC assembled in grana core, and a thylakoid membrane-bound FtsH2 metalloprotease that promotes O-triggered signaling through the proteolysis of EXECUTER1 (EX1) proteins associated with PSII in grana margin. The role of FtsH2 protease in O signaling was established recently in the conditional () mutant of that generates O upon dark-to-light shift. The mutant lacking functional FtsH2 significantly impairs O-triggered and EX1-mediated cell death. In the present study, the role of FtsH2 in the induction of O signaling was further clarified by analyzing the FtsH2-dependent nuclear gene expression changes in the mutant. Genome-wide transcriptome analysis showed that the inactivation of FtsH2 repressed the majority (85%) of the EX1-dependent O-responsive genes (SORGs), providing direct connection between FtsH2-mediated EX1 degradation and O-triggered gene expression changes. Furthermore, the overlap between β-CC-induced genes and EX1-FtsH2-dependent genes was very limited, further supporting the coexistence of two distinctive O signaling pathways.
光系统II反应中心（PSII RC）和捕光复合体不可避免地会产生具有高度反应活性的单线态氧（O），这种单线态氧会造成光氧化损伤，尤其是当产生速率超过解毒速率时。除了具有毒性外，单线态氧还被认为会触发逆行信号传导，从而导致核基因表达发生变化。似乎有两种不同的分子成分参与调节单线态氧信号传导：一种是在类囊体基粒核心组装的PSII RC中，单线态氧氧化β-胡萝卜素时产生的挥发性信号分子β-环柠檬醛（β-CC）；另一种是类囊体膜结合的FtsH2金属蛋白酶，它通过对类囊体边缘与PSII相关的EXECUTER1（EX1）蛋白进行蛋白水解，促进由单线态氧触发的信号传导。FtsH2蛋白酶在单线态氧信号传导中的作用最近在 的条件性（）突变体中得到证实，该突变体在从黑暗转变为光照时会产生单线态氧。缺乏功能性FtsH2的突变体显著损害了由单线态氧触发的以及EX1介导的细胞死亡。在本研究中，通过分析突变体中FtsH2依赖的核基因表达变化，进一步阐明了FtsH2在单线态氧信号诱导中的作用。全基因组转录组分析表明，FtsH2的失活抑制了大多数（85%）依赖EX1的单线态氧响应基因（SORGs），这为FtsH2介导的EX1降解与单线态氧触发的基因表达变化之间提供了直接联系。此外，β-CC诱导的基因与EX1 - FtsH2依赖的基因之间的重叠非常有限，这进一步支持了两种不同的单线态氧信号传导途径的共存。
