AtMYB44通过调节内源H2S合成参与植物响应盐胁迫的分子机制

H2S是近几年发现的重要气体信号分子，外源H2S提高植物抗逆性方面已有很多报道，但是对植物在响应逆境过程中内源H2S合成调控机制的了解非常有限。我们前期研究显示，盐胁迫下来自L/D-半胱氨酸脱巯基酶（LCD和DCD）途径的H2S水平明显升高，H2S合成突变体（lcd、dcd、lcd/dcd）均对盐的敏感性增强；转录因子myb44突变体与前者表型相似，且AtLCD和AtDCD基因表达下调、内源H2S含量下降、H2S合成酶活性降低；利用酵母单杂交证明AtMYB44与AtLCD和AtDCD启动子互作。这些结果强烈暗示了AtMYB44通过H2S信号对植物耐盐能力的调节作用。本项目拟在以上基础上，继续深入鉴定AtMYB44调控AtLCD和AtDCD的关键顺式作用元件，从体内和体外试验证实两者的结合受到了盐胁迫的调控，并进一步探究其响应盐胁迫的机制，为解析内源H2S参与盐胁迫的作用机制提供依据。

Hydrogen sulfide (H2S) is an important gaseous signal molecule. There are lots of reports presenting that the exogenous H2S participates in many plant physiological processes, especially in environmental stress responses. However, the study about the endogenous H2S in stress responses is limited. We previously found that in Arabidopsis, the endogenous H2S, synthesised from L-/D-cysteine desulphydrase (LCD and DCD), displayed a higher level under the salt treatment. The H2S biosynthesis mutants (lcd, dcd and lcd/dcd) were more sensitive to salt stress. In addition, we found that the transcription factor myb44 mutant showed salt sensitive phenotype, decreased gene expression of AtLCD and AtDCD, less H2S content, and inhibited H2S synthetase activity in the mutant. Further study indicated that the MYB44 transcription factor can bind to the promoter of AtLCD and AtDCD. These data suggested that AtMYB44 might regulate plant salt stress response through H2S signaling. In the study, we plan to identify the MYB44-regulated key cis elements of AtLCD and AtDCD, and analyze the binding regulation by the salt stress in vitro and in vivo. This study would not only greatly enhance our understanding of the molecular mechanism of how MYB44 regulating AtLCD and AtDCD genes expression to affect endogenous H2S synthesis, but also lay theoretical basis for the endogenous H2S participating in salt stress response.