FtsH2-Dependent Proteolysis of EXECUTER1 Is Essential in Mediating Singlet Oxygen-Triggered Retrograde Signaling in Arabidopsis thaliana.
FtsH2-Dependent Proteolysis of EXECUTER1 Is Essential in Mediating Singlet Oxygen-Triggered Retrograde Signaling in Arabidopsis thaliana.
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EXECUTER1 的 FtsH2 依赖性蛋白水解对于介导拟南芥中单线态氧触发的逆行信号传导至关重要
DOI：
10.3389/fpls.2017.01145
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发表时间：
2017
影响因子：
5.6
通讯作者：
Kim C
中科院分区：
文献类型：
--
作者：
Dogra V;Duan J;Lee KP;Lv S;Liu R;Kim C
光系统II反应中心(PSII RC)和捕光复合体不可避免地产生高活性的单线态氧(1O2)，造成光氧化损伤，特别是当生成速率超过解毒速率时。除了有毒外，1O2还被认为可以触发逆行信号，从而导致核基因表达的变化。两个不同的分子成分似乎调节1O2信号：一个是挥发性信号分子β-cycLocitral(β-CC)，它是在基粒核心组装的PSII RC中由1o2氧化β-胡萝卜素产生的；另一个是类囊体膜结合的FtsH2金属蛋白酶，它通过与基粒边缘的PSII相关的Executer1(EX1)蛋白的蛋白分解来促进1O2触发的信号转导。FtsH2蛋白水解酶在1O2信号转导中的作用最近在拟南芥的条件荧光(Flu)突变体中被证实，该突变体在从暗到光的转变中产生1O2。缺乏功能性FtsH2的流感突变体显著损害1O2触发和EX1介导的细胞死亡。在本研究中，通过分析依赖于FtsH2的核基因在流感突变体中的表达变化，进一步阐明了FtsH2在诱导1O2信号转导中的作用。全基因组转录组分析表明，FtsH2的失活抑制了大部分(85%)依赖EX1的1o2反应基因(SORGs)，提供了FtsH2介导的EX1降解和1o2触发的基因表达变化之间的直接联系。此外，β-CC诱导的基因和EX1-FtsH2依赖的基因之间的重叠非常有限，进一步支持了两条不同的1O2信号通路的共存。
Photosystem II reaction center (PSII RC) and light-harvesting complex inevitably generate highly reactive singlet oxygen (1O2) that can impose photo-oxidative damage, especially when the rate of generation exceeds the rate of detoxification. Besides being toxic, 1O2 has also been ascribed to trigger retrograde signaling, which leads to nuclear gene expression changes. Two distinctive molecular components appear to regulate 1O2 signaling: a volatile signaling molecule β-cyclocitral (β-CC) generated upon oxidation of β-carotene by 1O2 in PSII RC assembled in grana core, and a thylakoid membrane-bound FtsH2 metalloprotease that promotes 1O2-triggered signaling through the proteolysis of EXECUTER1 (EX1) proteins associated with PSII in grana margin. The role of FtsH2 protease in 1O2 signaling was established recently in the conditional fluorescent (flu) mutant of Arabidopsis thaliana that generates 1O2 upon dark-to-light shift. The flu mutant lacking functional FtsH2 significantly impairs 1O2-triggered and EX1-mediated cell death. In the present study, the role of FtsH2 in the induction of 1O2 signaling was further clarified by analyzing the FtsH2-dependent nuclear gene expression changes in the flu mutant. Genome-wide transcriptome analysis showed that the inactivation of FtsH2 repressed the majority (85%) of the EX1-dependent 1O2-responsive genes (SORGs), providing direct connection between FtsH2-mediated EX1 degradation and 1O2-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 1O2 signaling pathways.