State Key Laboratory of Crop Biology, College of Life Sciences, Shandong Agricultural University, Tai'an 271018, China.
Key Laboratory of Photobiology, Institute of Botany, Chinese Academy of Science, Beijing 100093, China.
Mol Plant. 2016 Apr 4;9(4):541-57. doi: 10.1016/j.molp.2015.12.013. Epub 2015 Dec 20.
myo-Inositol-1-phosphate synthase (MIPS) catalyzes the limiting step of inositol biosynthesis and has crucial roles in plant growth and development. In response to stress, the transcription of MIPS1 is induced and the biosynthesis of inositol or inositol derivatives is promoted by unknown mechanisms. Here, we found that the light signaling protein FAR-RED ELONGATED HYPOCOTYL3 (FHY3) and its homolog FAR-RED IMPAIRED RESPONSE1 (FAR1) regulate light-induced inositol biosynthesis and oxidative stress responses by activating the transcription of MIPS1. Disruption of FHY3 and FAR1 caused light-induced cell death after dark-light transition, precocious leaf senescence, and increased sensitivity to oxidative stress. Reduction of salicylic acid (SA) accumulation by overexpression of SALICYLIC ACID 3-HYDROXYLASE largely suppressed the cell death phenotype of fhy3 far1 mutant plants, suggesting that FHY3- and FAR1-mediated cell death is dependent on SA. Furthermore, comparative analysis of chromatin immunoprecipitation sequencing and microarray results revealed that FHY3 and FAR1 directly target both MIPS1 and MIPS2. The fhy3 far1 mutant plants showed severely decreased MIPS1/2 transcript levels and reduced inositol levels. Conversely, constitutive expression of MIPS1 partially rescued the inositol contents, caused reduced transcript levels of SA-biosynthesis genes, and prevented oxidative stress in fhy3 far1. Taken together, our results indicate that the light signaling proteins FHY3 and FAR1 directly bind the promoter of MIPS1 to activate its expression and thereby promote inositol biosynthesis to prevent light-induced oxidative stress and SA-dependent cell death.
肌醇-1-磷酸合酶（MIPS）催化肌醇生物合成的限速步骤，在植物生长发育中具有重要作用。在受到胁迫时，MIPS1 的转录被诱导，通过未知机制促进肌醇或肌醇衍生物的生物合成。在这里，我们发现光信号蛋白 FAR-RED ELONGATED HYPOCOTYL3（FHY3）及其同源物 FAR-RED IMPAIRED RESPONSE1（FAR1）通过激活 MIPS1 的转录来调节光诱导的肌醇生物合成和氧化应激反应。FHY3 和 FAR1 的缺失导致暗-光转换后光诱导的细胞死亡、过早的叶片衰老和对氧化应激的敏感性增加。通过过量表达 SALICYLIC ACID 3-HYDROXYLASE 减少水杨酸（SA）积累，在很大程度上抑制了 fhy3 far1 突变体植物的细胞死亡表型，表明 FHY3 和 FAR1 介导的细胞死亡依赖于 SA。此外，染色质免疫沉淀测序和微阵列结果的比较分析表明，FHY3 和 FAR1 直接靶向 MIPS1 和 MIPS2。fhy3 far1 突变体植物的 MIPS1/2 转录本水平严重降低，肌醇水平降低。相反，MIPS1 的组成型表达部分挽救了肌醇含量，降低了 SA 生物合成基因的转录本水平，并防止了 fhy3 far1 中的氧化应激。总之，我们的结果表明，光信号蛋白 FHY3 和 FAR1 直接结合 MIPS1 的启动子以激活其表达，从而促进肌醇生物合成，以防止光诱导的氧化应激和依赖 SA 的细胞死亡。
