查尔酮合酶
拟南芥
转录因子
MYB公司
查尔酮
活性氧
突变体
类黄酮生物合成
生物
生物化学
黄烷酮
调节器
细胞生物学
生物合成
类黄酮
植物
化学
基因表达
基因
转录组
抗氧化剂
立体化学
作者
Baozhu Li,Ruonan Fan,Siyi Guo,Pengtao Wang,Xiaohong Zhu,Yanting Fan,Yuxue Chen,Kai-Yue He,Arvind Kumar,Junping Shi,Ying Wang,Luhan Li,Zhubing Hu,Chun‐Peng Song
标识
DOI:10.1016/j.envexpbot.2019.103807
摘要
Salt stress is an adverse environmental factor severely disturbing plant growth and development. Correspondingly, plants have evolved in a set of machinery to cope with salt toxicity including transcriptional regulation. In this study, by employing knockout and overproducing plants, we found that MYB111 is a positive regulator in salt stress response. MYB111 deficiency significantly decreased salt tolerance in Arabidopsis, whereas MYB111 overproduction dramatically increased during the stages of seed germination and seedling growth. Physiological analyses suggested that this altered sensitivity may be from different reactive oxygen species (ROS) scavenging capacity. ROS accumulation was higher in myb111 mutants than the wild-type (WT) plants, but lower in MYB111-overexpressed plants. Consistent to previous report that MYB111 is a regulator in flavonoid synthesis, flavonoid accumulation was lower in mutants, but higher in MYB111-overexpressed plants compared with WT. Surprisingly, addition of bioflavonoids, chalcone/ dihydrokaempferole/ quercetin were able to rescue the loss of salt tolerance in myb111 mutants, demonstrating that flavonoids are crucial against salt stress. Furthermore, we found that MYB111 can bind to specific cis-elements in promoter of chalcone synthase (CHS), flavanone carboxylase (F3H), flavonol synthase 1 (FLS1), and in turn activates their transcription. Meanwhile, MYB111 expression was highly induced under salt treatment, indicating its role in responses to salt stress. Taken together, our data clearly showed that MYB111’s role on salt resistance is dependent on its regulation on flavonoid synthesis.
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