Na^(+)/K^(+)-ATPase is a transmembrane protein that has important roles in the maintenance of electrochemical gradients across cell membranes by transporting three Na^(+)out of and two K^(+)into cells.Additionally,Na^...Na^(+)/K^(+)-ATPase is a transmembrane protein that has important roles in the maintenance of electrochemical gradients across cell membranes by transporting three Na^(+)out of and two K^(+)into cells.Additionally,Na^(+)/K^(+)-ATPase participates in Ca^(2+)-signaling transduction and neurotransmitter release by coordinating the ion concentration gradient across the cell membrane.Na^(+)/K^(+)-ATPase works synergistically with multiple ion channels in the cell membrane to form a dynamic network of ion homeostatic regulation and affects cellular communication by regulating chemical signals and the ion balance among different types of cells.Therefo re,it is not surprising that Na^(+)/K^(+)-ATPase dysfunction has emerged as a risk factor for a variety of neurological diseases.However,published studies have so far only elucidated the important roles of Na^(+)/K^(+)-ATPase dysfunction in disease development,and we are lacking detailed mechanisms to clarify how Na^(+)/K^(+)-ATPase affects cell function.Our recent studies revealed that membrane loss of Na^(+)/K^(+)-ATPase is a key mechanism in many neurological disorders,particularly stroke and Parkinson's disease.Stabilization of plasma membrane Na^(+)/K^(+)-ATPase with an antibody is a novel strategy to treat these diseases.For this reason,Na^(+)/K^(+)-ATPase acts not only as a simple ion pump but also as a sensor/regulator or cytoprotective protein,participating in signal transduction such as neuronal autophagy and apoptosis,and glial cell migration.Thus,the present review attempts to summarize the novel biological functions of Na^(+)/K^(+)-ATPase and Na^(+)/K^(+)-ATPase-related pathogenesis.The potential for novel strategies to treat Na^(+)/K^(+)-ATPase-related brain diseases will also be discussed.展开更多
Salinity,a major abiotic stress,reduces plant growth and severely limits agricultural productivity.Plants regulate salt uptake via calcineurin B-like proteins(CBLs).Although extensive studies of the functions of CBLs ...Salinity,a major abiotic stress,reduces plant growth and severely limits agricultural productivity.Plants regulate salt uptake via calcineurin B-like proteins(CBLs).Although extensive studies of the functions of CBLs in response to salt stress have been conducted in Arabidopsis,their functions in Setaria italica are still poorly understood.The foxtail millet genome encodes seven CBLs,of which only SiCBL4 was shown to be involved in salt response.Overexpression of SiCBL5 in Arabidopsis thaliana sos3-1 mutant rescued its salt hypersensitivity phenotype,but that of other SiCBLs(SiCBL1,SiCBL2,SiCBL3,SiCBL6,and SiCBL7)did not rescue the salt hypersensitivity of the Atsos3-1 mutant.SiCBL5 harbors an N-myristoylation motif and is located in the plasma membrane.Overexpression of SiCBL5 in foxtail millet increased its salt tolerance,but its knockdown increased salt hypersensitivity.Yeast two-hybrid and firefly luciferase complementation imaging assays showed that SiCBL5 physically interacted with SiCIPK24 in vitro and in vivo.Cooverexpression of SiCBL5,SiCIPK24,and SiSOS1 in yeast conferred a high-salt-tolerance phenotype.Compared to wild-type plants under salt stress conditions,SiCBL5 overexpressors showed lower accumulations of Na^(+) and stronger Na^(+) efflux,whereas RNAi-SiCBL5 plants showed higher accumulations of Na^(+) and weaker Na^(+) efflux.These results indicate that SiCBL5 confers salt tolerance in foxtail millet by modulating Na^(+) homeostasis.展开更多
Rice(Oryza sativa L.)is a staple cereal for more than two thirds of the world's population.Soil salinity severely limits rice growth,development,and grain yield.It is desirable to elucidate the mechanism of rice&#...Rice(Oryza sativa L.)is a staple cereal for more than two thirds of the world's population.Soil salinity severely limits rice growth,development,and grain yield.It is desirable to elucidate the mechanism of rice's salt-stress response.As the major source of H_(2)O_(2),NADPH oxidase(Rboh)is believed to be involved in salt-stress tolerance.However,the function and mechanism of rice Rboh in salt stress response remain unclear.In this study,we found that the expression of OsRbohA was up-regulated by NaCl treatment in the shoots and roots of rice seedlings.Knockout of OsRbohA reduced the tolerance of rice to salt stress.Knockout of OsRbohA blocked NaCl-induced increases of NADPH activity and H_(2)O_(2) content in roots.OsRboh A knockout inhibited root growth and disrupted K^(+)homeostasis by reducing the expression of K^(+) transporters and channel-associated genes(OsGORK,OsAKT1,OsHAK1,and OsHAK5)in roots under NaCl treatment.Under NaCl treatment,OsRbohA knockout also reduced subcellular K^(+) contents of the plasma membrane and soluble fraction.Overexpression of OsRbohA increased the expression of K^(+) transporters and channel-associated genes and reduced the loss of K^(+) ions in roots.These results indicate that OsRboh A-mediated H_(2)O_(2) accumulation modulates K^(+) homeostasis,thereby increasing salt tolerance in rice.展开更多
基金supported by the National Natural Science Foundation of China,No.82173800 (to JB)Shenzhen Science and Technology Program,No.KQTD20200820113040070 (to JB)。
文摘Na^(+)/K^(+)-ATPase is a transmembrane protein that has important roles in the maintenance of electrochemical gradients across cell membranes by transporting three Na^(+)out of and two K^(+)into cells.Additionally,Na^(+)/K^(+)-ATPase participates in Ca^(2+)-signaling transduction and neurotransmitter release by coordinating the ion concentration gradient across the cell membrane.Na^(+)/K^(+)-ATPase works synergistically with multiple ion channels in the cell membrane to form a dynamic network of ion homeostatic regulation and affects cellular communication by regulating chemical signals and the ion balance among different types of cells.Therefo re,it is not surprising that Na^(+)/K^(+)-ATPase dysfunction has emerged as a risk factor for a variety of neurological diseases.However,published studies have so far only elucidated the important roles of Na^(+)/K^(+)-ATPase dysfunction in disease development,and we are lacking detailed mechanisms to clarify how Na^(+)/K^(+)-ATPase affects cell function.Our recent studies revealed that membrane loss of Na^(+)/K^(+)-ATPase is a key mechanism in many neurological disorders,particularly stroke and Parkinson's disease.Stabilization of plasma membrane Na^(+)/K^(+)-ATPase with an antibody is a novel strategy to treat these diseases.For this reason,Na^(+)/K^(+)-ATPase acts not only as a simple ion pump but also as a sensor/regulator or cytoprotective protein,participating in signal transduction such as neuronal autophagy and apoptosis,and glial cell migration.Thus,the present review attempts to summarize the novel biological functions of Na^(+)/K^(+)-ATPase and Na^(+)/K^(+)-ATPase-related pathogenesis.The potential for novel strategies to treat Na^(+)/K^(+)-ATPase-related brain diseases will also be discussed.
基金supported by the National Natural Science Foundation of China(32001445 and 31871534)the Natural Science Foundation of Jiangsu Province(BK20200557)。
文摘Salinity,a major abiotic stress,reduces plant growth and severely limits agricultural productivity.Plants regulate salt uptake via calcineurin B-like proteins(CBLs).Although extensive studies of the functions of CBLs in response to salt stress have been conducted in Arabidopsis,their functions in Setaria italica are still poorly understood.The foxtail millet genome encodes seven CBLs,of which only SiCBL4 was shown to be involved in salt response.Overexpression of SiCBL5 in Arabidopsis thaliana sos3-1 mutant rescued its salt hypersensitivity phenotype,but that of other SiCBLs(SiCBL1,SiCBL2,SiCBL3,SiCBL6,and SiCBL7)did not rescue the salt hypersensitivity of the Atsos3-1 mutant.SiCBL5 harbors an N-myristoylation motif and is located in the plasma membrane.Overexpression of SiCBL5 in foxtail millet increased its salt tolerance,but its knockdown increased salt hypersensitivity.Yeast two-hybrid and firefly luciferase complementation imaging assays showed that SiCBL5 physically interacted with SiCIPK24 in vitro and in vivo.Cooverexpression of SiCBL5,SiCIPK24,and SiSOS1 in yeast conferred a high-salt-tolerance phenotype.Compared to wild-type plants under salt stress conditions,SiCBL5 overexpressors showed lower accumulations of Na^(+) and stronger Na^(+) efflux,whereas RNAi-SiCBL5 plants showed higher accumulations of Na^(+) and weaker Na^(+) efflux.These results indicate that SiCBL5 confers salt tolerance in foxtail millet by modulating Na^(+) homeostasis.
基金supported by the National Natural Science Foundation of China(31671606,31971824)Postgraduate Research and Practice Innovation Program of Jiangsu Province(KYCX18_0743)。
文摘Rice(Oryza sativa L.)is a staple cereal for more than two thirds of the world's population.Soil salinity severely limits rice growth,development,and grain yield.It is desirable to elucidate the mechanism of rice's salt-stress response.As the major source of H_(2)O_(2),NADPH oxidase(Rboh)is believed to be involved in salt-stress tolerance.However,the function and mechanism of rice Rboh in salt stress response remain unclear.In this study,we found that the expression of OsRbohA was up-regulated by NaCl treatment in the shoots and roots of rice seedlings.Knockout of OsRbohA reduced the tolerance of rice to salt stress.Knockout of OsRbohA blocked NaCl-induced increases of NADPH activity and H_(2)O_(2) content in roots.OsRboh A knockout inhibited root growth and disrupted K^(+)homeostasis by reducing the expression of K^(+) transporters and channel-associated genes(OsGORK,OsAKT1,OsHAK1,and OsHAK5)in roots under NaCl treatment.Under NaCl treatment,OsRbohA knockout also reduced subcellular K^(+) contents of the plasma membrane and soluble fraction.Overexpression of OsRbohA increased the expression of K^(+) transporters and channel-associated genes and reduced the loss of K^(+) ions in roots.These results indicate that OsRboh A-mediated H_(2)O_(2) accumulation modulates K^(+) homeostasis,thereby increasing salt tolerance in rice.
