Ethylene Response Factors are transcription factors that act as a key regulatory hub in plant response to abiotic stresses, integrating ethylene, ABA, jasmonate
Leaf senescence is a highly regulated physiological process that leads to leaf death and is, as such, the last developmental stage of the leaf. Plant aging and environmental stresses may induce the process of senescence. Here we will focus on the role of leaf senescence in field-grown plants as a response to adverse climatic conditions and, more specifically, on how it contributes to plant survival under drought stress. Drought induces several responses in plants including leaf senescence, which plays a major role in the survival of several species. Drought-induced leaf senescence contributes to nutrient remobilisation during stress, thus allowing the rest of the plant (i.e. the youngest leaves, fruits or flowers) to benefit from the nutrients accumulated during the life span of the leaf. In addition, drought-induced leaf senescence, especially when accompanied by leaf abscission, avoids large losses through transpiration, thus contributing to the maintenance of a favourable water balance of the whole plant. Drought-induced leaf senescence occurs gradually and is characterised by specific macroscopic, cellular, biochemical and molecular changes. Leaf yellowing (i.e. chlorophyll degradation) and specific changes in cell ultrastructure (e.g. chromatin condensation, thylakoid swelling, plastoglobuli accumulation), metabolism (e.g. protein degradation, lipid peroxidation) and gene expression occur during leaf senescence in drought-stressed plants. Cytokinins and ABA have been shown to be involved in the regulation of drought-induced leaf senescence, although the possible role of other plant hormones should not be excluded. Reactive oxygen species, whose concentrations increase during drought-induced leaf senescence, are also known to be regulators of this process. The complex mechanisms of regulation of leaf senescence in drought-stressed plants are discussed, and attention is drawn to those aspects that still require investigation.
The transition from juvenility through maturation to senescence is a complex process that involves the regulation of longevity. Here, we identify JUNGBRUNNEN1 (JUB1), a hydrogen peroxide (H2O2)-induced NAC transcription factor, as a central longevity regulator in Arabidopsis thaliana. JUB1 overexpression strongly delays senescence, dampens intracellular H2O2 levels, and enhances tolerance to various abiotic stresses, whereas in jub1-1 knockdown plants, precocious senescence and lowered abiotic stress tolerance are observed. A JUB1 binding site containing a RRYGCCGT core sequence is present in the promoter of DREB2A, which plays an important role in abiotic stress responses. JUB1 transactivates DREB2A expression in mesophyll cell protoplasts and transgenic plants and binds directly to the DREB2A promoter. Transcriptome profiling of JUB1 overexpressors revealed elevated expression of several reactive oxygen species–responsive genes, including heat shock protein and glutathione S-transferase genes, whose expression is further induced by H2O2 treatment. Metabolite profiling identified elevated Pro and trehalose levels in JUB1 overexpressors, in accordance with their enhanced abiotic stress tolerance. We suggest that JUB1 constitutes a central regulator of a finely tuned control system that modulates cellular H2O2 level and primes the plants for upcoming stress through a gene regulatory network that involves DREB2A.