Abiotic Stresses Intervene with ABA Signaling to Induce Destructive Metabolic Pathways Leading to Death: Premature Leaf Senescence in Plants

Abstract

Abiotic stresses trigger premature leaf senescence by affecting some endogenous factors, which is an important limitation for plant growth and grain yield. Among these endogenous factors that regulate leaf senescence, abscisic acid (ABA) works as a link between the oxidase damage of cellular structure and signal molecules responding to abiotic stress during leaf senescence. Considering the importance of ABA, we collect the latest findings related to ABA biosynthesis, ABA signaling, and its inhibitory effect on chloroplast structure destruction, chlorophyll (Chl) degradation, and photosynthesis reduction. Post-translational changes in leaf senescence end with the exhaustion of nutrients, yellowing of leaves, and death of senescent tissues. In this article, we review the literature on the ABA-inducing leaf senescence mechanism in rice and Arabidopsis starting from ABA synthesis, transport, signaling receptors, and catabolism. We also predict the future outcomes of investigations related to other plants. Before changes in translation occur, ABA signaling that mediates the expression of NYC, bZIP, and WRKY transcription factors (TFs) has been investigated to explain the inducing effect on senescence-associated genes. Various factors related to calcium signaling, reactive oxygen species (ROS) production, and protein degradation are elaborated, and research gaps and potential prospects are presented. Examples of gene mutation conferring the delay or induction of leaf senescence are also described, and they may be helpful in understanding the inhibitory effect of abiotic stresses and effective measures to tolerate, minimize, or resist their inducing effect on leaf senescence.

Keywords: ABA biosynthesis; ABA signaling receptors; ABA-induced transcription factors; chlorophyll degradation; premature leaf senescence.

Figure 1

Abscisic acid (ABA) biosynthesis, ABA catabolism, and ABA signaling sensors (receptors) pathways. SAG: senescence-associated gene, In MEP (Methyl Erythritol Phosphate), β-carotene is converted into zeaxanthin, ZFP (zeaxanthin epoxidase) catalyze zeaxanthin into violaxanthin, NSY (neo xanthin synthase) convert violaxanthin into neo xanthin and 9 cis-violaxanthin, NCED (9-cis-epoxycarotenoid dioxygenase) convert 9 cis-violaxanthin into xanthocin and then abscisic aldehyde, ABAO: abscisic aldehyde oxidase catalyzes abscisic aldehyde into abscisic acid. ABA is sensed by ABA receptors; PYL (pyrabactin resistance 1-like), PP2C (protein phosphatase 2C) which activate SnRK2. The activated SnRK2 phosphorylate ABFs (ABA-responsive element-binding factors) to induce the expression of SAGs (senescence-associated genes).

Figure 2

A schematic diagram of ABA signal transduction toward chlorophyll degradation and reduced photosynthetic activity. ( indicate induction and indicates suppression). Abiotic stresses induce ABA production, which is sensed by ABA signaling receptors (ABF, PYL). ABA signal induce expression of NAC, bZIP and NYC TFs. The activated TFs induce expression of SAGs which are translated in RBs (ribosomes) to synthesize (NOL, NADPH oxidase, Chl-b reductase). NDPH oxidase increase ROS production and Chl b reductase reduce PSII (photosystem II) efficiency and induce the degradation of D1 protein.

Figure 3

Systematic illustration of ABA-induced leaf senescence in response to abiotic stresses. DET1: DE-ETIOLATED1, ABC: ATP-binding cassette, TOR: target of rapamycin, bHLH: basic helix-loop-helix TF, Rbohf: respiratory burst oxidative homolog.