Photoinduced reactive oxygen species(ROS)-based pollutant removal is one of the ideal solutions to achieve the conversion of solar energy into chemical energy and thus to address environmental pollution.Here,earthabun...Photoinduced reactive oxygen species(ROS)-based pollutant removal is one of the ideal solutions to achieve the conversion of solar energy into chemical energy and thus to address environmental pollution.Here,earthabundant CaCO_(3)-decorated g-C_(3)N_(4)(g-C_(3)N_(4)labeled as CN,CaCO_(3)-decorated g-C_(3)N_(4)sample labeled as CN-CCO)has been constructed by a facile thermal polymerization method for safe and efficient photocatalytic NO removal.The decorated CaCO_(3)as“transit hub”extends theπbonds of CN to deviate from the planes and steers the random charge carriers,which thus provides extra active sites and expedites spatial charge separation to facilitate adsorption/activation of reactants and promote formation of ROS participating in the removal of pollutant.Furthermore,boosted generation of ROS regulates the photocatalytic NO oxidation pathway and thus increases the selectivity of products.NO prefers to be directly oxidized into final product(nitrate)rather than toxic intermediates(NO_(2)),which is well demonstrated by theoretically simulated ROS-based reaction pathways and experimental characterization.The present work promotes the degradation of pollutant and simultaneously suppresses the formation of toxic by-product,which paves the way for ROS-based pollutant removal.展开更多
Reactive oxygen species （ROS） play an important role in root responses to potassium deprivation by regulating the expression of the high-affinity K＋ transporter gene AtHAK5 and other genes. Activation-tagged lines ...Reactive oxygen species （ROS） play an important role in root responses to potassium deprivation by regulating the expression of the high-affinity K＋ transporter gene AtHAK5 and other genes. Activation-tagged lines of Arabidopsis plants containing the AtHAK5 promoter driving luciferase were screened for bioluminescence under potassium- sufficient conditions. A member of the type Ill peroxidase family, RCI3, was isolated and when it was overexpressed by the activation tag, this led to the enhanced expression of luciferase and the endogenous AtHAKS. RCI3 was found to be up- regulated upon potassium deprivation. Plants overexpressing RCI3 （RCI3-ox） showed more ROS production and AtHAK5 expression whereas the ROS production and AtHAK5 expression were reduced in rci3-1 under K＋-deprived conditions. These results suggested that RCI3 is involved in the production of ROS under potassium deprivation and that RCI3- mediated ROS production affects the regulation of AtHAK5 expression. This peroxidase appears to be another component of the low-potassium signal transduction pathway in Arabidopsis roots.展开更多
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
Effector-triggered immunity(ETI)in plants is mediated by intracellular nucleotide-binding leucine-rich repeat receptors(NLRs),which converge on calcium(Ca^(2+))signaling pathways.However,how NLR-induced Ca^(2+)signals...Effector-triggered immunity(ETI)in plants is mediated by intracellular nucleotide-binding leucine-rich repeat receptors(NLRs),which converge on calcium(Ca^(2+))signaling pathways.However,how NLR-induced Ca^(2+)signals initiate downstream immune responses,such as enhancing reactive oxygen species(Ros)signaling,remains largely unclear.In this study,we identified a calcium-dependent protein kinase(CPK)that regulates sustained ROS signaling during ETI.We found that,upon infection with Pseudomonas syringae pv.tomato(Pst)DC3000(avrRpm1),cPK12 is activated in a Ca^(2+)-dependent manner and governs the transport of ETl-RoS from the apoplast to cytoplasm.Both in vitro and in vivo phosphorylation assays revealed that CPK12 phosphorylates theplasma membrane intrinsic protein PiP2;1,thereby enhancing Ros transport and elevating plant resistance to Pst Dc3000(avrRpm1).Taken together,our findings demonstrate that CPK12 deciphers effector-triggered Ca^(2+) signals to regulate ROS compartmentalization,establishing a crucial link between NLR-mediated Ca2+signaling and the spatial control of RoS responses inplantimmunity.展开更多
Stimuli-responsive delivery systems hold promise in cancer treatments.However,their application potential has been limited due to undesirable drug leaking during blood circulation and inefficient therapeutic efficacy ...Stimuli-responsive delivery systems hold promise in cancer treatments.However,their application potential has been limited due to undesirable drug leaking during blood circulation and inefficient therapeutic efficacy in tumors,resulting in undesirable therapeutic outcomes.Herein,we have developed a novel redox-sensitive pegylated phospholipid,termed as DOPE-SS-PEG,which can form a glutathione(GSH)-triggered precision explosive system(GPS)for simultaneously improving circulation stability,tumor specificity,and chemosensitivity,leading to explosive anticancer effects.GPS is constructed of liposomal doxorubicin(DOX)functionalized with DOPE-SS-PEG and MnO_(2) nanoparticles,which can protect liposome structure in the presence of serum GSH(20μM),whereas converts to cationic liposome in response to intracellular GSH(10 mM),thereby enhancing circulation stability,tumor specificity,endosomal escape,and cytoplasmic delivery.Importantly,GPS can not only generate oxygen to relieve hypoxia and consequently enhance chemosensitivity,but quench GSH antioxidability to elevate the accruement of intracellular reactive oxygen species(ROS),leading to an explosion of oxidative stress induced cell injury.Particularly,in vivo studies show that GPS selectively accumulates in tumor tissues,effectively inhibits tumor growth,exhibits minimal systemic adverse effects,and consequently prolongs the survival time of tumor-bearing mice.Therefore,GPS is a unique stimuli-responsive treatment with programmed and on-demand drug delivery,as well as explosive therapeutic efficacy,and provides an intelligent anticancer treatment.展开更多
基金supported by the National Natural Science Foundation of China(Grant Nos.21822601,21777011)the Fundamental Research Funds for the Central Universities(ZYGX2019Z021)+2 种基金the 111 Project(B20030)the Southwest Petroleum University Graduate Research Innovation Fund Project(2019cxzd008)Shanghai Tongji Gao Tingyao Environmental Science&Technology Development Foundation。
文摘Photoinduced reactive oxygen species(ROS)-based pollutant removal is one of the ideal solutions to achieve the conversion of solar energy into chemical energy and thus to address environmental pollution.Here,earthabundant CaCO_(3)-decorated g-C_(3)N_(4)(g-C_(3)N_(4)labeled as CN,CaCO_(3)-decorated g-C_(3)N_(4)sample labeled as CN-CCO)has been constructed by a facile thermal polymerization method for safe and efficient photocatalytic NO removal.The decorated CaCO_(3)as“transit hub”extends theπbonds of CN to deviate from the planes and steers the random charge carriers,which thus provides extra active sites and expedites spatial charge separation to facilitate adsorption/activation of reactants and promote formation of ROS participating in the removal of pollutant.Furthermore,boosted generation of ROS regulates the photocatalytic NO oxidation pathway and thus increases the selectivity of products.NO prefers to be directly oxidized into final product(nitrate)rather than toxic intermediates(NO_(2)),which is well demonstrated by theoretically simulated ROS-based reaction pathways and experimental characterization.The present work promotes the degradation of pollutant and simultaneously suppresses the formation of toxic by-product,which paves the way for ROS-based pollutant removal.
文摘Reactive oxygen species （ROS） play an important role in root responses to potassium deprivation by regulating the expression of the high-affinity K＋ transporter gene AtHAK5 and other genes. Activation-tagged lines of Arabidopsis plants containing the AtHAK5 promoter driving luciferase were screened for bioluminescence under potassium- sufficient conditions. A member of the type Ill peroxidase family, RCI3, was isolated and when it was overexpressed by the activation tag, this led to the enhanced expression of luciferase and the endogenous AtHAKS. RCI3 was found to be up- regulated upon potassium deprivation. Plants overexpressing RCI3 （RCI3-ox） showed more ROS production and AtHAK5 expression whereas the ROS production and AtHAK5 expression were reduced in rci3-1 under K＋-deprived conditions. These results suggested that RCI3 is involved in the production of ROS under potassium deprivation and that RCI3- mediated ROS production affects the regulation of AtHAK5 expression. This peroxidase appears to be another component of the low-potassium signal transduction pathway in Arabidopsis roots.
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.
基金supported by the National Natural Science Foundation of China(32470284 and 32270289)Natural Science Foundation of Zhejiang Province,China(Z25C140005)+1 种基金Key Research and Development Program of Zhejiang Province,China(2024SsYS0104 and 2021C02064-7)National Key Research and Development Program of China(2023YFD1902903).
文摘Effector-triggered immunity(ETI)in plants is mediated by intracellular nucleotide-binding leucine-rich repeat receptors(NLRs),which converge on calcium(Ca^(2+))signaling pathways.However,how NLR-induced Ca^(2+)signals initiate downstream immune responses,such as enhancing reactive oxygen species(Ros)signaling,remains largely unclear.In this study,we identified a calcium-dependent protein kinase(CPK)that regulates sustained ROS signaling during ETI.We found that,upon infection with Pseudomonas syringae pv.tomato(Pst)DC3000(avrRpm1),cPK12 is activated in a Ca^(2+)-dependent manner and governs the transport of ETl-RoS from the apoplast to cytoplasm.Both in vitro and in vivo phosphorylation assays revealed that CPK12 phosphorylates theplasma membrane intrinsic protein PiP2;1,thereby enhancing Ros transport and elevating plant resistance to Pst Dc3000(avrRpm1).Taken together,our findings demonstrate that CPK12 deciphers effector-triggered Ca^(2+) signals to regulate ROS compartmentalization,establishing a crucial link between NLR-mediated Ca2+signaling and the spatial control of RoS responses inplantimmunity.
基金This work were supported by the National Key Research and Development Program of China(No.2019YFA0802800)the National Key Research and Development Program of China(No.2018YFB1105400)+3 种基金the National Natural Science Foundation of China(No.21472090)the Natural Science Foundation of Jiangsu Province(No.BK20180334)the Fundamental Research Funds for Central Universities Nanjing University,the Scientific Research Foundation of Graduate School of Nanjing University(No.2018CL12)The Key Research and Development Program of Jiangsu Provincial Department of Science and Technology of China(No.BE2019002).
文摘Stimuli-responsive delivery systems hold promise in cancer treatments.However,their application potential has been limited due to undesirable drug leaking during blood circulation and inefficient therapeutic efficacy in tumors,resulting in undesirable therapeutic outcomes.Herein,we have developed a novel redox-sensitive pegylated phospholipid,termed as DOPE-SS-PEG,which can form a glutathione(GSH)-triggered precision explosive system(GPS)for simultaneously improving circulation stability,tumor specificity,and chemosensitivity,leading to explosive anticancer effects.GPS is constructed of liposomal doxorubicin(DOX)functionalized with DOPE-SS-PEG and MnO_(2) nanoparticles,which can protect liposome structure in the presence of serum GSH(20μM),whereas converts to cationic liposome in response to intracellular GSH(10 mM),thereby enhancing circulation stability,tumor specificity,endosomal escape,and cytoplasmic delivery.Importantly,GPS can not only generate oxygen to relieve hypoxia and consequently enhance chemosensitivity,but quench GSH antioxidability to elevate the accruement of intracellular reactive oxygen species(ROS),leading to an explosion of oxidative stress induced cell injury.Particularly,in vivo studies show that GPS selectively accumulates in tumor tissues,effectively inhibits tumor growth,exhibits minimal systemic adverse effects,and consequently prolongs the survival time of tumor-bearing mice.Therefore,GPS is a unique stimuli-responsive treatment with programmed and on-demand drug delivery,as well as explosive therapeutic efficacy,and provides an intelligent anticancer treatment.
