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.

Highlights

  • Leaf senescence is an age-dependent programmed cell death that propels nutrients from aging cells to developing and storage tissues and causes the exhausted materials to accumulate in dying cells [1,2]

  • Leaf senescence is a temporal niche with integrated aging and phytohormone regulatory factors

  • The dominating environmental stresses intervene with phytohormone regulatory factors to trigger and/or accelerate leaf senescence, which is a limiting factor of quantitative and qualitative traits

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Summary

Introduction

Leaf senescence is an age-dependent programmed cell death that propels nutrients from aging cells to developing and storage tissues and causes the exhausted materials to accumulate in dying cells [1,2]. The increased catabolic activity is responsible for converting the cellular materials of the growth phase of leaves into exportable nutrients that are supplied to developing seeds or other growing organs. This natural leaf senescence is responsible for the continuity of life by transferring nutrients and genetic information from generation to generation [5]. The integrated mechanism of abiotic factors with ABA for the induction of premature leaf senescence, covering the chloroplast degradation and photosynthesis decline, ROS generation and oxidative stress, kinase protein regulation, and secondary messenger Ca2+ are discussed. Our review covers recent findings about the interaction of ABA with carbon and sugar signaling as well as ethylene to induce leaf senescence

ABA Biosynthesis and Catabolism
ABA Transport
ABA Signaling Receptors
Integrated Mechanism of ABA-Induced Leaf Senescence
ABA Modulates Leaf Senescence by Activating Regulating Kinase Protein
Modulating OsNAC2 TF Expression
Regulation of bZIP TF
Gene Mutation as the Key Step to Identify ABA Regulation for Senescence
Interaction of Sugar Signaling with ABA during Leaf Senescence
Interacted Crosstalk between Ethylene and ABA
Findings
Conclusions and Future Recommendations
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