Leaf senescence can be triggered by various abiotic stresses.Among these,heat stress emerges as a pivotal environmental factor,particularly in light of the predicted rise in global temperatures.However,the molecular m...Leaf senescence can be triggered by various abiotic stresses.Among these,heat stress emerges as a pivotal environmental factor,particularly in light of the predicted rise in global temperatures.However,the molecular mechanism underlying heat-induced leaf senescence remains largely unexplored.As a cool-season grass species,tall fescue(Festuca arundinacea)is an ideal and imperative material for investigating heat-induced leaf senescence because heat stress easily triggers leaf senescence to influence its forage yield and turf quality.Here,we investigated the role of FaNAC047 in heat-induced leaf senescence.Overexpression of FaNAC047 promoted heat-induced leaf senescence in transgenic tall fescue that was evidenced by a more seriously destructive photosystem and higher accumulation of reactive oxygen species(ROS),whereas knockdown of FaNAC047 delayed leaf senescence.Further protein-DNA interaction assays indicated that FaNAC047 directly activated the transcriptions of NON-YELLOW COLORING 1(FaNYC1),NYC1-like(FaNOL),and STAY-GREEN(FaSGR)but directly inhibited Catalases 2(FaCAT2)expression,thereby promoting chlorophyll degradation and ROS accumulation.Subsequently,protein-protein interaction assays revealed that FaNAC047 physically interacted with FaNAC058 to enhance its regulatory effect on FaNYC1,FaNOL,FaSGR,and FaCAT2.Additionally,FaNAC047 could transcriptionally activate FaNAC058 expression to form a regulatory cascade,driving senescence progression.Consistently,the knockdown of FaNAC058 significantly delayed heat-induced leaf senescence.Collectively,our results reveal that FaNAC047-FaNAC058 module coordinately mediates chlorophyll degradation and ROS production to positively regulate heat-induced leaf senescence.The findings illustrate the molecular network of heat-induced leaf senescence for breeding heat-resistant plants.展开更多
基金National Natural Science Foundation of China(NSFC)(Grant Nos.32471765,32101430,and 32441039)the Major Science and Technology Innovation Project of Shandong Province(No.2022LZGC018)+2 种基金the National Science Foundation for Distinguished Young Scholars of Hubei Province(No.2021CFA060)International Science and Technology Cooperation Project of Hubei Province(No.2021EHB021)the Science&Technology Specific Projects in Agricultural Hightech Industrial Demonstration Area of the Yellow River Delta(No.2022SZX13).
文摘Leaf senescence can be triggered by various abiotic stresses.Among these,heat stress emerges as a pivotal environmental factor,particularly in light of the predicted rise in global temperatures.However,the molecular mechanism underlying heat-induced leaf senescence remains largely unexplored.As a cool-season grass species,tall fescue(Festuca arundinacea)is an ideal and imperative material for investigating heat-induced leaf senescence because heat stress easily triggers leaf senescence to influence its forage yield and turf quality.Here,we investigated the role of FaNAC047 in heat-induced leaf senescence.Overexpression of FaNAC047 promoted heat-induced leaf senescence in transgenic tall fescue that was evidenced by a more seriously destructive photosystem and higher accumulation of reactive oxygen species(ROS),whereas knockdown of FaNAC047 delayed leaf senescence.Further protein-DNA interaction assays indicated that FaNAC047 directly activated the transcriptions of NON-YELLOW COLORING 1(FaNYC1),NYC1-like(FaNOL),and STAY-GREEN(FaSGR)but directly inhibited Catalases 2(FaCAT2)expression,thereby promoting chlorophyll degradation and ROS accumulation.Subsequently,protein-protein interaction assays revealed that FaNAC047 physically interacted with FaNAC058 to enhance its regulatory effect on FaNYC1,FaNOL,FaSGR,and FaCAT2.Additionally,FaNAC047 could transcriptionally activate FaNAC058 expression to form a regulatory cascade,driving senescence progression.Consistently,the knockdown of FaNAC058 significantly delayed heat-induced leaf senescence.Collectively,our results reveal that FaNAC047-FaNAC058 module coordinately mediates chlorophyll degradation and ROS production to positively regulate heat-induced leaf senescence.The findings illustrate the molecular network of heat-induced leaf senescence for breeding heat-resistant plants.
