Soybean(Glycine max)is one of the most important food crops and oil crops in the world.According to the role of sucrose transporter in sugar accumulation,GmTST2.1(Glyma.04G000300)and ZmGIF1 of sugar transport related ...Soybean(Glycine max)is one of the most important food crops and oil crops in the world.According to the role of sucrose transporter in sugar accumulation,GmTST2.1(Glyma.04G000300)and ZmGIF1 of sugar transport related genes were separately overexpressed in the soybean cultivar Heihe 43 from the perspective of regulatory source to library relationship in the study.The function of soluble sugar accumulation in grains layed a theoretical foundation for the cultivation of new varieties of high-yield genetically modified soybeans.The results showed that the height and 100-seed weight of the over-expressed GmTST2.1 gene were increased with 7%and 17.7%and the soluble sugar content was increased with 1.575 times as much as that of the wild-type soybean.The overexpressed ZmGIF1 gene was found to be 10%higher than that of plant height,1.8%higher than that of 100-seed weight and larger seed size and 1.3 times higher than that of soluble sugar content.Biological yields were increased in both GmTST2.1 and ZmGIF1 genes.展开更多
As a member of the inwardly rectifying channel (Kir) family, Kir2.1 allows to influx the cell more easily than to efflux, a biophysical phenomenon named inward rectification. The function of Kir2.1 is to set the resti...As a member of the inwardly rectifying channel (Kir) family, Kir2.1 allows to influx the cell more easily than to efflux, a biophysical phenomenon named inward rectification. The function of Kir2.1 is to set the resting membrane potential and modulate membrane excitability. It has been reported that residue E224 plays a key role in regulating inward rectification. The mutant Kir2.1 (E224G) displays weaker inward rectification than the WT channel. Gating of Kir2.1 depends on the membrane lipid, PIP<sub>2</sub>, such that the channel gates are closed in the absence of PIP<sub>2</sub>. Here we perform electrophysiological and computational approaches, and demonstrate that E224 also plays an important role in the PIP<sub>2</sub>-dependent activation of Kir2.1 in addition to its influence on inward rectification. The E224G mutant takes 4.5 times longer to be activated by PIP<sub>2</sub>. To probe the mechanism by which E224G slows the channel opening kinetics, we perform targeted molecular dynamics simulations and find that the mutant weakens the interactions between CD-loop and C-linker (H221-R189) and the adjacent G-loops (R312-E303) which are thought to stabilize the open state of the channel in our previous work. These data provide new insights into the regulation of Kir2.1 channel activity and suggest that a common mechanism may be involved in the distinct biophysical processes, such as inward rectification and PIP<sub>2</sub>-induced gating.展开更多
We find that a conserved mutation residue Glu to residue Asp (E303D), which both have the same polar and charged properties, makes Kit2.1 protein lose its function. To understand the mechanism, we identify three int...We find that a conserved mutation residue Glu to residue Asp (E303D), which both have the same polar and charged properties, makes Kit2.1 protein lose its function. To understand the mechanism, we identify three interactions which control the conformation change and maintain the function of the Kit2.1 protein by combining homology modeling and molecular dynamics with targeted molecular dynamics. We find that the E303D mutation weakens these interactions and results in the loss of the related function. Our data indicate that not only the amino residues but also the interactions determine the function of proteins.展开更多
基金Supported by Heilongjiang Provincial Project(Topic JC2018007,GX17B002,C2018016,GJ2018GJ0098)Chinese National Natural Science Foundation(31671717)+1 种基金the Postdoctoral Fund in Heilongjiang Province(LBH-Z15017,LBH-Q17015)the National Project(CARS-04-PS04)。
文摘Soybean(Glycine max)is one of the most important food crops and oil crops in the world.According to the role of sucrose transporter in sugar accumulation,GmTST2.1(Glyma.04G000300)and ZmGIF1 of sugar transport related genes were separately overexpressed in the soybean cultivar Heihe 43 from the perspective of regulatory source to library relationship in the study.The function of soluble sugar accumulation in grains layed a theoretical foundation for the cultivation of new varieties of high-yield genetically modified soybeans.The results showed that the height and 100-seed weight of the over-expressed GmTST2.1 gene were increased with 7%and 17.7%and the soluble sugar content was increased with 1.575 times as much as that of the wild-type soybean.The overexpressed ZmGIF1 gene was found to be 10%higher than that of plant height,1.8%higher than that of 100-seed weight and larger seed size and 1.3 times higher than that of soluble sugar content.Biological yields were increased in both GmTST2.1 and ZmGIF1 genes.
基金Supported by the National Natural Science Foundation for Distinguished Young Scholars of Hebei Province under Grant Nos C2015202340 and C2013202244the Foundation for Outstanding Talents of Hebei Province under Grant No C201400305+3 种基金the National Natural Science Foundation of China under Grant Nos 11247010,11175055,11475053,11347017,31400711 and 11647121the NIH R01 under Grant No HL059949-18the Foundation for the Science and Technology Program of Higher Education Institutions of Hebei Province under Grant No QN2016113the Scientific Innovation Fund for Excellent Young Scientists of Hebei University of Technology under Grant No 2015010
文摘As a member of the inwardly rectifying channel (Kir) family, Kir2.1 allows to influx the cell more easily than to efflux, a biophysical phenomenon named inward rectification. The function of Kir2.1 is to set the resting membrane potential and modulate membrane excitability. It has been reported that residue E224 plays a key role in regulating inward rectification. The mutant Kir2.1 (E224G) displays weaker inward rectification than the WT channel. Gating of Kir2.1 depends on the membrane lipid, PIP<sub>2</sub>, such that the channel gates are closed in the absence of PIP<sub>2</sub>. Here we perform electrophysiological and computational approaches, and demonstrate that E224 also plays an important role in the PIP<sub>2</sub>-dependent activation of Kir2.1 in addition to its influence on inward rectification. The E224G mutant takes 4.5 times longer to be activated by PIP<sub>2</sub>. To probe the mechanism by which E224G slows the channel opening kinetics, we perform targeted molecular dynamics simulations and find that the mutant weakens the interactions between CD-loop and C-linker (H221-R189) and the adjacent G-loops (R312-E303) which are thought to stabilize the open state of the channel in our previous work. These data provide new insights into the regulation of Kir2.1 channel activity and suggest that a common mechanism may be involved in the distinct biophysical processes, such as inward rectification and PIP<sub>2</sub>-induced gating.
基金Supported by the National Natural Science Foundation of China under Grant Nos 11247010,11175055,11475053 and 11347017the Natural Science Foundation of Hebei Province under Grant Nos C2012202079 and C201400305
文摘We find that a conserved mutation residue Glu to residue Asp (E303D), which both have the same polar and charged properties, makes Kit2.1 protein lose its function. To understand the mechanism, we identify three interactions which control the conformation change and maintain the function of the Kit2.1 protein by combining homology modeling and molecular dynamics with targeted molecular dynamics. We find that the E303D mutation weakens these interactions and results in the loss of the related function. Our data indicate that not only the amino residues but also the interactions determine the function of proteins.