Uncoupled Expression of Nuclear and Plastid Photosynthesis-Associated Genes Contributes to Cell Death in a Lesion Mimic Mutant
Uncoupled Expression of Nuclear and Plastid Photosynthesis-Associated Genes Contributes to Cell Death in a Lesion Mimic Mutant
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核和质体光合作用相关基因的解偶联表达导致损伤模拟突变体的细胞死亡
DOI：
10.1105/tpc.18.00813
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发表时间：
2019-01-01
期刊：
影响因子：
11.6
通讯作者：
Kim, Chanhong
中科院分区：
文献类型：
--
作者：
Lv, Ruiqing;Li, Zihao;Kim, Chanhong
叶绿体到核的逆行信号是光合作用相关核基因(PhANGs)和叶绿体基因(PhAPGs)耦合表达的关键，以确保植物叶绿体(CP)的功能状态。虽然在拟南芥中已经鉴定了参与这一过程的各种信号成分，但这种协调的生物学意义仍然是一个谜。在这里，我们证明了PhANGs和PhAPGs的解偶联表达导致了拟南芥的病变模拟疾病1(LSD1)突变体的细胞死亡。水杨酸(SA)的日长依赖性增加似乎在细胞死亡开始之前迅速上调LSD1中编码Sigma因子结合蛋白1(SIB1)的基因，SIB1是一种转录辅助调节因子。SIB1双靶向细胞核和CPS导致PhANGs的上调和PhAPGs的下调。因此，这扰乱了光合作用蛋白质的化学计量，特别是在PSII中，导致在CPS中产生高活性的单线态氧(O-1(2))。因此，核编码的CP蛋白EXECUTER1(可能是O-1(2)传感器)的失活显著减弱了LSD1诱导的细胞死亡。综上所述，这些结果提供了一条从SA-到O-1(2)-信号通路的途径，这两条通路通过PhANGs和PhAPGs的解偶联表达而交织在一起，有助于LSD1中模拟细胞死亡的损伤。
Chloroplast-to-nucleus retrograde signaling is essential for the coupled expression of photosynthesis-associated nuclear genes (PhANGs) and plastid genes (PhAPGs) to ensure the functional status of chloroplasts (Cp) in plants. Although various signaling components involved in the process have been identified in Arabidopsis (Arabidopsis thaliana), the biological relevance of such coordination remains an enigma. Here, we show that the uncoupled expression of PhANGs and PhAPGs contributes to the cell death in the lesion simulating disease1 (lsd1) mutant of Arabidopsis. A daylength-dependent increase of salicylic acid (SA) appears to rapidly up-regulate a gene encoding SIGMA FACTOR BINDING PROTEIN1 (SIB1), a transcriptional coregulator, in lsd1 before the onset of cell death. The dual targeting of SIB1 to the nucleus and the Cps leads to a simultaneous up-regulation of PhANGs and down-regulation of PhAPGs. Consequently, this disrupts the stoichiometry of photosynthetic proteins, especially in PSII, resulting in the generation of the highly reactive species singlet oxygen (O-1(2)) in Cps. Accordingly, inactivation of the nuclear-encoded Cp protein EXECUTER1, a putative O-1(2) sensor, significantly attenuates the lsd1-conferred cell death. Together, these results provide a pathway from the SA-to the O-1(2) -signaling pathway, which are intertwined via the uncoupled expression of PhANGs and PhAPGs, contributing to the lesionmimicking cell death in lsd1.