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Molecular mechanisms of abiotic stress-induced senescence in plants
- Acronym AbioSen
- Duration 36
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Project leader
Müller-Röber,Bernd (PL),Germany Potsdam U
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Other project participants
van Breusegem, Frank Belgium U Ghent / Gent
Gechev, Tsanko Bulgaria "Institute of Molecular Biology and Biotechnology
(IMBB), Plovdiv"
Hörtensteiner, Stefan Switzerland U Zürich
- Funding
- Total Granted budget ca. € 638.600
Abstract
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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 oxidativeand 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 analysed 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 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. |
