Premature leaf senescence is a major constraint on rice (Oryza sativa L.) productivity and yield stability, particularly under increasingly frequent environmental stresses. Unlike developmentally programmed senescence, premature senescence is characterized by early and uncontrolled activation of senescence pathways, leading to accelerated chlorophyll degradation, oxidative damage, impaired photosynthesis, and reduced grain filling. Recent studies have revealed that premature senescence in rice is governed by a complex regulatory network integrating reactive oxygen species (ROS) homeostasis, phytohormone signaling, transcriptional regulation, and environmental cues. Central signaling hubs involving abscisic acid, ethylene, jasmonic acid, cytokinins, and gibberellins interact extensively with ROS metabolism to fine-tune senescence onset and progression. These upstream signals converge on key transcription factor families, particularly NAC and WRKY proteins, which directly regulate senescence-associated genes responsible for chloroplast dismantling, nutrient remobilization, and programmed cell death. Moreover, abiotic stresses such as drought, salinity, temperature extremes, and nitrogen deficiency commonly trigger premature senescence through a shared ABA–ROS signaling module. This review systematically summarizes recent advances in the physiological characteristics, molecular mechanisms, and environmental regulation of premature leaf senescence in rice, and discusses emerging genetic and agronomic strategies to delay senescence. A deeper understanding of senescence regulatory networks will facilitate the development of rice cultivars with prolonged photosynthetic duration, improved stress resilience, and enhanced yield stability under changing climatic conditions.
Sun et al. (Wed,) studied this question.