背景回顾：GOLDEN2-LIKE (GLK) transcription factors drive the expression of photosynthesis-associated nuclear genes (PhANGs) indispensable for chloroplast biogenesis. Salicylic acid (SA)-induced SIGMA FACTOR-BINDING PROTEIN 1 (SIB1), a transcription coregulator and positive regulator of cell death, interacts with GLK1 and GLK2 to reinforce the expression of PhANGs, leading to photoinhibition of photosystem II and singlet oxygen (¹O₂) burst in chloroplasts. 1O2 then contributes to SA-induced cell death via EXECUTER 1 (EX1, 1O2 sensor protein)-mediated retrograde signaling upon reaching a critical level. 

研究问题：This earlier finding has initiated research on the potential role of GLK1/2 and EX1 inSA signaling. 

主要发现：Consistent with this view, we reveal that LESION-SIMULATING DISEASE 1 (LSD1), a transcription coregulator and negative regulator of SA-primed cell death, interacts with GLK1/2 to repress their activities in Arabidopsis (Arabidopsis thaliana). 

结果1-过表达和功能缺失：Overexpression of LSD1 repressed GLK target genes, including PhANGs, whereas loss of LSD1 enhanced their expression. Remarkably, LSD1 overexpression inhibited chloroplast biogenesis, resembling the characteristic glk1glk2 double mutant phenotype. 

结果2-LSD1-GLK：Subsequent chromatin immunoprecipitation coupled with expression analyses further revealed that LSD1 inhibits the DNA-binding activity of GLK1 towards its target promoters. 

结果3-SIB1与LSD1拮抗：SA-induced nuclear-targeted SIB1 proteins appeared to interrupt the LSD1-GLK interaction, and the subsequent SIB1-GLK interaction activated EX1-mediated 1O2 signaling, elucidating antagonistic modules SIB1 and LSD1 in the regulation of GLK activity. 

结论：Taken together, we provide a working model that SIB1 and LSD1, mutually exclusive SA-signaling components, antagonistically regulate GLK1/2 to fine-tune the expression of PhANGs, thereby modulating 1O2 homeostasis and related stress responses.

 摘 要 

GLK转录因子驱动光合相关核基因（PhANGs）的表达，对于叶绿体的发育是不可或缺的。受水杨酸诱导的转录共调控子SIB1正调控细胞死亡，该基因能够与GLK1/2发生互作，从而增强PhANGs的表达，导致光系统II的光抑制以及叶绿体中的单态氧爆发。接着，单态氧通过单态氧感知蛋白EX1介导的逆行信号作用于水杨酸诱导的细胞死亡。这些发现开启了对于GLK1/2和EX1在水杨酸信号转导功能方面的研究。与此一致，作者发现在拟南芥中，转录共调控因子、水杨酸诱导的细胞死亡的正调控因子LSD1能够与GLK1/2互作，抑制GLK1/2的活性。过表达LSD1会抑制PhANGs等GLK靶向基因的表达，而LSD1的功能缺失会增强这些基因的表达。重要的是，LSD1过表达会抑制叶绿体生物发生，这与glk1glk2双突的表型缺陷类似。后续的染色质免疫共沉淀和表达分析表明，LSD1抑制了GLK1蛋白结合到靶标基因启动子上的DNA结合活性。水杨酸诱导的核靶向SIB1蛋白能够扰乱LSD1-GLK的互作，随后SIB1-GLK互作激活了EX1介导的单态氧信号转导，表明SIB1和LSD1蛋白在GLK活性调控方面存在拮抗作用。综上，本文的研究揭示了互不相容的水杨酸信号转导组分SIB1和LSD1蛋白拮抗调控GLK1/2，从而精细调控PhANGs的表达，最终调节单态氧的内稳态及相关的胁迫响应。

 通讯作者 

** Chanhong Kim **