| Leaf senescence is a natural age-dependent process that is induced prematurely by various internal and environmental stresses. At this developmental stage, leaf senescence has a strong impact on important agronomical traits such as seed yield, as well as seed protein and lipid contents. Previous studies indicated that oxidative stress plays an important role in the regulation of progress of senescence in plants. Also, it has been reported that almost all of the autophagy-defective mutants not only have an early senescence phenotype under nutrient-rich conditions, but also could down-regulated catalase activity and in turn increases H2O2 accumulation. Autophagy is an evolutionarily conserved intracellular degradation process whereby cytoplasmic components are degraded in the vacuole to provide raw materials and energy and also to eliminate damaged or toxic components for the maintenance of essential cellular functions. However, it is unclear whether autophagy-regulated oxidative stress could affect leaf senescence. For this, genetics, metabolomics and physiological approaches are employed to investigate the crosstalk between autophagy and oxidative in the regulation of senescence. Furthermore, our work demonstrates that under high level of CO2, the early senescence phenotype of autophagy defective mutant (atg2, atg5 and atg18a) was accelerated further. When plants were grown to an age of six weeks in air, at which point early senescence is apparent in atg single mutants, no senescence was observed in cat2 atg double mutants. Also, single atg2 and double cat2 atg2 mutants were grown for four weeks in high CO2, at which point early senescence is initiated in atg2, and then transferred to air to induce oxidative stress in cat2 genotypes and grown for a further week. This analysis revealed that whereas the atg2 single mutant develops obvious senescence on the outer leaves, this phenotype was less apparent in cat2 atg2. These analyses revealed that whereas the atg single mutant develops obvious senescence on the outer leaves, this phenotype was less apparent in cat2 atg mutant. Taken together, these results indicate that oxidative stress originating from excess photorespiratory H2O2 can act antagonistically to the early senescence induced in atg mutants. Also, this phenotype of early senescence in these mutants might be triggered by either other cellular sources of ROS or ROS independent pathways or both. Meanwhile, the study may provide a theoretical basis for improving the quality of agricultural products.H2S has been reported involved in various physiological processes of plant growth and development, such as seed germination, root development, stomatal apertures, osmotic stress, salt stress, oxidative stress, metal stresse, pathogen challenge, heat stress, freezing tolance, post harvest. Recently, DES1 is the only identified L-Cys desulfhydrate located in the cytosol, which degrades the L-Cys to H2S, ammonia and pyruvate. Here, we chose the model plant Arabidopsis thaliana as a research system, using genetics, physiology to explore the role of H2S in the H2O2-triggered signal transduction. The results showed that H2S content and LCD activity of the 21-day cat2 mutant were significantly higher than Col-0, and the H2S content, LCD activity and the lesion of the rosette leaf increased significantly through the treatment of continuous exogenous NaHS donor in cat2 mutant. H2S content was decreased, but the lesion of the rosette leaf was significantly decreased of cat2 desl double mutant compared with that of cat2 mutant. Further, analysis of the antioxidase activity and antioxidants, there’s no significant difference between cat2 mutant and cat2 desl double mutant. We concluded that H2S generated by DES1 in the cytosol positively regulate H2O2-mediated cell death of leaves, which is no correlation with the glutathione-mediated redox system. |
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