Molecular mechanisms of abiotic stress-induced senescence in plants

极端温度、脱水、饥饿和黑暗等非生物胁迫因素可以诱导大多数植物的早衰。 植物是例如耐干燥的植物物种，如Haberlea rhodopensis。在这些情况下，非生物胁迫诱导的衰老被延迟或消除。我们对各种压力如何最终触发有害的衰老过程的知识仍然很少。AbioSen项目的主要目标是绘制和研究将非生物胁迫衍生信号整合到衰老途径中的复杂网络。一个多方面的方法，包括正向和反向遗传学，结合高通量转录组，蛋白质组和代谢组分析将实施。AbioSen组织在4个工作包（WP）：WP 1，解开转录因子（TF）的基因调控网络，调节氧化和非生物胁迫诱导的衰老在A。thaliana.通过ChIP-seq，RNA-seq和ChIP-蛋白质组学的组合，将分析两个转录因子（RD 26，ATAF 1）的全球基因调控网络，这些转录因子受衰老和氧化/非生物胁迫的调控，并依赖于非生物（干旱，盐）胁迫控制叶片衰老。WP 2，在发育和胁迫诱导的衰老过程中研究叶绿素分解的基因调控网络。thaliana.将鉴定和表征靶向叶绿素（Chl）分解代谢基因的TF。NAC因子SHYG被P1鉴定为CYP 89 A9的上游调节因子。 P2以前证明CYP 89 A9是叶绿素分解代谢酶。其他转录调节因子将通过使用基因组学和基于LC-MS的代谢组学的新方法的财团的协调行动来确定。这将允许鉴定用于植物衰老诱导的诊断分子和代谢物标记。WP 3，构建过氧化氢诱导的失绿/细胞死亡/衰老的遗传网络。增加的H2 O2水平触发防御反应和细胞死亡。从EMS诱变的过氧化氢酶缺陷型拟南芥植物获得的10个可用回复突变体中的致病突变将被鉴定，并在功能上表征与其应激反应和衰老表型相关的特征。WP 4，衰老的分子机制。玫瑰花属高分辨率时间转录组和代谢组分析黑暗诱导的衰老在H。将进行rhodopensis，以获得可能参与衰老过程的基因和代谢物的清单。编码衰老相关蛋白（包括调节叶绿素降解的保绿蛋白）的基因将使用计算和功能方法进行进一步研究。来自4个WP的综合数据将增加我们对依赖非生物胁迫调节植物衰老的基本机制的了解，并将为未来的作物育种提供有价值的见解。

Abiotic stress factors like extreme temperatures, dehydration, starvation, and darkness, can induce premature senescence in most plants. Exceptions are e.g. desiccation-tolerant plant species like Haberlea rhodopensis. In these, abiotic stress induced senescence is delayed or abolished. Our knowledge on how a variety of stresses finally trigger the detrimental senescence process is still scarce. The main objective of the AbioSen project is to chart and study the intricate network that integrates abiotic stress-derived signals into the senescence pathway. A multifaceted approach including forward and reverse genetics, combined with high-throughput transcriptome, proteome, and metabolome analyses will be implemented. AbioSen is organised in 4 work packages (WP): WP1, Unravelling the gene regulatory networks of transcription factors (TFs) that modulate oxidative- and abiotic stress-induced senescence in A. thaliana. The global gene regulatory networks of two transcription factors (RD26, ATAF1) that are regulated by both senescence and oxidative/abiotic stress and which control leaf senescence in dependence on abiotic (drought, salinity) stress will be analyzed through a combination of ChIP-seq, RNA-seq and ChIP-proteomics. WP2, Investigating the gene regulatory network of chlorophyll breakdown during developmental and stress-induced senescence in A. thaliana. TFs that target chlorophyll (Chl) catabolic genes will be identified and characterized. The NAC factor SHYG was identified by P1 as an upstream regulator of CYP89A9. P2 demonstrated before that CYP89A9 is chlorophyll catabolic enzyme. Additional transcriptional regulators will be identified through a concerted action of the consortium using genomics and a new method for LC-MS-based metabolomics. This will allow the identification of diagnostic molecular and metabolite markers for senescence induction in plants. WP3, Framing a genetic network of hydrogen peroxide-induced chlorosis/cell death/senescence. Increased H2O2 levels trigger defence responses and cell death. Causative mutations in ten available revertants obtained from EMS-mutagenized catalase deficient Arabidopsis plants will be identified and functionally characterised in relation to their stress responses and senescence phenotype. WP4, Molecular mechanisms of senescence in H. rhodopensis. High-resolution temporal transcriptome and metabolome profiling of dark-induced senescence in H. rhodopensis will be carried out to obtain an inventory of genes and metabolites potentially involved in the senescence process. Genes encoding senescence-related proteins (including the stay-green proteins that regulate Chl degradation) will be further studied using computational and functional approaches. The integrated data from the 4 WPs will increase our knowledge about the fundamental mechanisms that regulate plant senescence in dependence of abiotic stress and will provide valuable insights for future crop breeding.