The C2H2-type zinc finger protein ZOS202 regulates leaf senescence in rice by targeting senescence-associated transcription factors and ROS homoeostasis.
TL;DR
It is shown that knockout mutation of the C2H2-type zinc finger TF gene ZOS202 resulted in delayed leaf senescence under both dark-induced and natural conditions, while overexpression lines exhibit accelerated leaf senescence, as indicated by reactive oxygen species overaccumulation, chloroplast degradation, and leaf cell death.
Abstract
Leaf senescence is a tightly regulated developmental process orchestrated by multiple transcription factor (TF) families. Although C2H2-type zinc finger proteins are known to participate in various aspects of plant growth and abiotic stress responses, their specific role in regulating leaf senescence remains poorly understood. Here, we show that knockout mutation of the C2H2-type zinc finger TF gene ZOS202 (LOC_Os02g02424) resulted in delayed leaf senescence under both dark-induced and natural conditions, while overexpression lines exhibit accelerated leaf senescence, as indicated by reactive oxygen species (ROS) overaccumulation, chloroplast degradation, and leaf cell death. As a dual-function transcription factor whose expression peaks at senescence onset, ZOS202 directly activates senescence-associated TF genes OsWRKY42, OsWRKY53, and ONAC096, while repressing peroxidase genes OsPRX113, OsPRX114, and OsPRX122, thereby disrupting ROS homeostasis and promoting senescence. Collectively, our findings uncover ZOS202 as a positive regulator of leaf senescence that acts by coordinating chlorophyll breakdown and ROS accumulation, providing promising strategies for fine-tuning leaf senescence in rice breeding.