Cross-talk between redox, metabolic and hormonal retrograde chloroplast signals in the expressional regulation of nuclear encoded plastid proteins

基于对调控动力学和相关转录因子的研究结果，以及在第一个资助期建立的方法，第二个阶段的工作计划侧重于表征代谢调节逆行信号的早期事件，特别是在光转移期间。(i)时间分辨的转录反应在野生型和定义的突变体与激素，氧化还原和代谢过程的缺陷将被用来解决组件的信号和代谢网络。(ii)逆行信号传导依赖于组合信号整合，如例如对于依赖于光、CO2和脱落酸的几种转录因子转录物水平所见。因此，该项目将研究光合作用相关的氧化还原，脱落酸和代谢物信号的组合效应，以确定信号的层次和整合。(iii)将在体外和体内研究鉴定的AP 2/EREBP家族和NAC转录因子的非常快速响应的转录调节因子的功能。(iv)转录本积累和蛋白量之间的差异表明转录后调节最有可能在逆行信号的控制下，这将使用FLAG表位标记的核糖体蛋白L18拟南芥系来比较总的和核糖体结合的mRNA。这将补充我们试图破译的氧化还原，脱落酸和代谢物线索在逆行信号在转录后水平的组合效应。

Based on the results on regulatory dynamics and involved transcription factors, and also on methods established in the first funding period, the work plan for the second period focuses on characterizing early events in retrograde signaling for metabolic adjustment, particularly during light shift. (i) Time-resolved transcriptional responses in wild type and defined mutants with defects in hormonal, redox and metabolite processes will be used to address components of the signaling and metabolic network. (ii) Retrograde signaling relies on combinatorial signal integration as seen e.g. for several transcription factor transcript level in dependence on light, CO2 and abscisic acid. Thus, the project will investigate the combinatorial effect of photosynthesis-related redox, abscisic acid and metabolite signals in order to define the signaling hierarchy and integration. (iii) The function of identified very fast responding transcriptional regulators of the AP2/EREBP family and a NAC transcription factor will be studied in vitro and in vivo. (iv) Discrepancies between transcript accumulation and protein amounts indicate posttranscriptional regulation being most likely under control of retrograde signals that will be addressed using FLAG-epitope tagged ribosomal protein L18 Arabidopsis lines to compare total and ribosome-bound mRNA. This will complement our attempt to decipher the combinatorial effect of redox, abscisic acid and metabolite cues in retrograde signaling at the posttranscriptional level.