Molecular mechanisms of abiotic stress-induced senescence in plants
非生物胁迫诱导植物衰老的分子机制
基本信息
- 批准号:263402999
- 负责人:
- 金额:--
- 依托单位:
- 依托单位国家:德国
- 项目类别:Research Grants
- 财政年份:2015
- 资助国家:德国
- 起止时间:2014-12-31 至 2018-12-31
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
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.
极端温度、脱水、饥饿和黑暗等非生物胁迫因素会导致大多数植物过早衰老。例外的是耐干燥的植物物种,如哈伯利亚。在这些情况下,非生物胁迫诱导的衰老被延缓或消除。我们对各种压力如何最终触发有害的衰老过程的了解仍然很少。ABioSen项目的主要目标是绘制和研究将非生物胁迫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被实施。ABioSen由4个工作包(WP)组成:WP1,揭开转录因子(TF)的基因调控网络,这些转录因子调节氧化和非生物胁迫诱导的A.thaliana衰老。两种转录因子(RD26、ATAF1)受衰老和氧化/非生物胁迫调节,并依赖于非生物(干旱、盐分)胁迫控制叶片衰老,将通过CHIP-SEQ、RNA-SEQ和CHIP-蛋白质组学相结合来分析这两个转录因子的全球基因调控网络。WP2,研究拟南芥发育和胁迫诱导衰老过程中叶绿素降解的基因调控网络。针对叶绿素(Chl)分解代谢基因的转录因子将被识别和表征。NAC因子SHYG被P1鉴定为CYP89A9的上游调控因子。P2证明了细胞色素P89A9是一种叶绿素分解代谢酶。将通过该联盟利用基因组学和一种基于LC-MS的代谢组学的新方法的协调行动来确定其他转录调控因子。这将有助于鉴定诱导植物衰老的诊断分子和代谢物标记。WP3,构建了过氧化氢诱导的黄化/细胞死亡/衰老的遗传网络。过氧化氢水平升高会引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株中获得的10个可用回复突变体中的致病突变将被鉴定,并从功能上描述其与胁迫反应和衰老表型的关系。WP4,黄花鱼衰老的分子机制。高分辨率的时间转录组和代谢组谱的黑暗诱导的衰老将被进行,以获得一个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Chl降解的持续绿色蛋白)的基因将利用计算和功能方法进一步研究。来自4个WPS的综合数据将增加我们对依赖于非生物胁迫调控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。
项目成果
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Professor Dr. Stefan Hörtensteiner (†)其他文献
Professor Dr. Stefan Hörtensteiner (†)的其他文献
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