Die and let live: leaf senescence contributes to plant survival under drought stress

Abstract

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.

Regulation of reactive oxygen species generation under drought conditions in Arabidopsis

“…10 Increased ROS levels also induce leaf senescence, contributing to the maintenance of water balance within the whole plant and nutrient remobilization to the youngest leaves or sink organs. 11 We found that the NTL4 gene is induced in the presence of H 2 O 2 , suggesting that the NTL4 gene would be related with ROS response and/or signaling. 5 In addition, endogenous contents of ROS were altered in the 35S:4ΔC transgenic plants and ntl4-1 mutants.…”

“…11 However, it is unknown how ROS metabolism is linked with the drought-induced leaf senescence. We found that when the pNTL4-GUS transgenic plants were exposed to water deficit, GUS activity was significantly leaf senescence was accelerated in the 35S:4ΔC transgenic plants, it was significantly delayed in the ntl4 mutants under drought conditions.…”

Overexpression of a LAM Domain Containing RNA-Binding Protein LARPIc Induces Precocious Leaf Senescence in Arabidopsis

“…Dramatic changes in cell structure and metabolism occur during leaf senescence, including the degradation of chloroplasts, mitochondria, and nuclei, and simultaneous catabolism of chlorophyll pigments, nucleic acids, proteins, and lipids. The nutrients released from senescing leaves are transported to newly-developing leaves, fruits, or seeds (Buchanan-Wollaston et al, 2005;Lim et al, 2007a;Munné-Bosch and Alegre, 2004).…”

ABA receptor PYL9 promotes drought resistance and leaf senescence

“…Recently, studies on transgenic tobacco showed that delayed leaf senescence increases plant resistance to drought stress (1). However, the senescence and abscission of older leaves and subsequent transfer of nutrients are known to increase plant survival under abiotic stresses, including drought, low or high temperatures, and darkness (2,3). Senescence mainly develops in an age-dependent manner and is also triggered by environmental stresses and phytohormones, such as abscisic acid (ABA), ethylene, salicylic acid, and jasmonic acid, but delayed by cytokinin (4).…”