COI1参与茉莉酸调控拟南芥吲哚族芥子油苷生物合成过程

芥子油苷是一类具有防御作用的植物次生代谢产物,外源激素茉莉酸对吲哚族芥子油苷的合成具有强烈的诱导作用,但茉莉酸调控吲哚族芥子油苷生物合成的分子机制并不清楚。以模式植物拟南芥(Arabidopsis thaliana)的野生型和coi1-22、coi1-23两种突变体为研究材料,通过茉莉酸甲酯(MeJA)处理,比较了拟南芥野生型和coi1突变体植株吲哚族芥子油苷含量、吲哚族芥子油苷合成前体色氨酸的生物合成基因(ASA1、TSA1和TSB1)、吲哚族芥子油苷生物合成基因(CYP79B2、CYP79B3和CYP83B1)及调控基因(MYB34和MYB51)的表达对MeJA的响应差异,由此确定茉莉酸信号通过COI1蛋白调控吲哚族芥子油苷生物合成,即茉莉酸信号通过信号开关COI1蛋白作用于转录因子MYB34和MYB51,进而调控吲哚族芥子油苷合成基因CYP79B2、CYP79B3、CYP83B1和前体色氨酸的合成基因ASA1、TSA1、TSB1。并且推断,COI1功能缺失后,茉莉酸信号可能通过其他未知调控因子或调控途径激活MYB34转录因子从而调控下游基因表达。     

Jasmonate mediates salt-induced nicotine biosynthesis in tobacco(Nicotiana tabacum L.)

Jasmonate(JA),as an important signal,plays a key role in multiple processes of plant growth,development and stress response.Nicotine and related pyridine alkaloids in tobacco(Nicotiana tabacum L.) are essential secondary metabolites.Whether environmental factors control nicotine biosynthesis and the underlying mechanism remains previously unreported.Here,we applied physiological and biochemical approaches to investigate how salt stress affects nicotine biosynthesis in tobacco.We found that salt stress induced the biosynthesis of JA,which subsequently triggered the activation of JA-responsive gene expression and,ultimately,nicotine synthesis.Bioinformatics analysis revealed the existence of many Nt MYC2a-recognized G-box motifs in the promoter regions of Nt LOX,Nt AOS,Nt AOC and Nt OPR genes.Applying exogenous JA increased nicotine content,while suppressing JA biosynthesis reduced nicotine biosynthesis.Salt treatment could not efficiently induce nicotine biosynthesis in transgenic anti-COI1 tobacco plants.These results demonstrate that JA acts as the essential signal which triggers nicotine biosynthesis in tobacco after salt stress.     

Jasmonate mediates salt induced nicotine biosynthesis in tobacco (Nicotiana tabacum L.)

Jasmonate (JA), as an important signal, plays a key role in multiple processes of plant growth, deve lopment and stress response. Nicotine and related pyridine alkaloids in tobacco (Nicotiana tabacum L.) are essential secondary metabolites. Whether environmental factors control nicotine biosynthesis and the underlying mechanism remains previously unreported. Here, we applied physiological and biochemical approaches to investigate how salt stress affects nicotine biosynthesis in tobacco. We found that salt stress induced the biosynthesis of JA, which subsequently triggered the activation of JA responsive gene expression and, ultimately, nicotine synthesis. Bioinformatics analysis revealed the existence of many NtMYC2a recognized G box motifs in the promoter regions of NtLOX, NtAOS, NtAOC and NtOPR genes. Applying exogenous JA increased nicotine content, while suppressing JA biosynthesis reduced nicotine biosynthesis. Salt treatment could not efficiently induce nicotine biosynthesis in transgenic anti COI1 tobacco plants. These results demonstrate that JA acts as the essential signal which triggers nicotine biosynthesis in tobacco after salt stress.