Chloroplasts are plant-specific organelles that evolved from endosymbiotic cyanobacteria. They divide through binary fission. Selection of the chloroplast division site is pivotal for the symmetric chloroplast divisio...Chloroplasts are plant-specific organelles that evolved from endosymbiotic cyanobacteria. They divide through binary fission. Selection of the chloroplast division site is pivotal for the symmetric chloroplast division. In E. coli, positioning of the division site at the midpoint of the cell is regulated by dynamic oscillation of the Min system, which includes MinC, MinD and MinE. Homologs of MinD and MinE in plants are involved in chloroplast division. The homolog of MinC still has not been identified in higher plants. However, an FtsZ-like protein, ARC3, was found to be involved in chloroplast division site positioning. Here, we report that chloroplast division site positioning 1 （AtCDP1） is a novel chloroplast division protein involved in chloroplast division site placement in Arabidopsis. AtCDP1 was discovered by screening an Arabidopsis cDNA expression library in bacteria for colonies with a cell division phenotype. AtCDP1 is exclusively expressed in young green tissues in Arabidopsis. Elongated chloroplasts with multiple division sites were observed in the loss-of-function cdpl mutant. Overexpression of AtCDP1 caused a chloroplast division phenotype too. Protein interaction assays suggested that AtCDP1 may mediate the chloroplast division site positioning through the interaction with ARC3. Overall, our results indicate that AtCDP1 is a novel component of the chloroplast division site positioning system, and the working mechanism of this system is different from that of the traditional MinCDE system in prokaryotic cells.展开更多
PHYTOCHROME INTERACTING FACTOR3 （PIF3） is an important component in the phytochrome signaling pathway and mediates plant responses to various environmental conditions. We found that PIF3 is involved in the inhibitio...PHYTOCHROME INTERACTING FACTOR3 （PIF3） is an important component in the phytochrome signaling pathway and mediates plant responses to various environmental conditions. We found that PIF3 is involved in the inhibition of root growth of Arabidopsis thaliana seedlings induced by nitric oxide （NO） in light. Overexpression of PIF3 partially alleviated the inhibitory effect of NO on root growth, whereas the pif3-1 mutant displayed enhanced sensitivity to NO in terms of root growth. During phytochrome signaling, the photoreceptor PHYB mediates the degradation of PIF3. We found that the phyB-9 mutant had a similar phenotype to that of PIF3ox in terms of responsiveness to NO. Furthermore, NO treatment promoted the accumulation of PHYB, and thus reduced PIF3 content. Our results further show that the activity of PIF3 is regulated by the DELLA protein RGL3[RGA （repressor of gal-3） LIKE 3]. Therefore, we speculate that PIF3 lies downstream of PHYB and RGL3, and plays an important role in the inhibitory effect of NO on root growth of Arabidopsis seedlings in light.展开更多
Sessile plants can adjust their growth and development in response to environmental stimuli.Sunlight(light),is the primary source of energy for all life on the earth,in the long course of phylogenetic evolution,plants...Sessile plants can adjust their growth and development in response to environmental stimuli.Sunlight(light),is the primary source of energy for all life on the earth,in the long course of phylogenetic evolution,plants have developed a unique relationship with light:they can absorb light energy and convert it into organic matter for use by themselves and others。展开更多
Nitrate-induced Ca^(2+) signaling is crucial for the primary nitrate response in plants.However,the molecular mechanism underlying the generation of the nitrate-specific calcium signature remains unknown.We report her...Nitrate-induced Ca^(2+) signaling is crucial for the primary nitrate response in plants.However,the molecular mechanism underlying the generation of the nitrate-specific calcium signature remains unknown.We report here that a cyclic nucleotide-gated channel(CNGC)protein,CNGC15,and the nitrate transceptor(NRT1.1)constitute a molecular switch that controls calcium influx depending on nitrate levels.The expression of CNGC15 is induced by nitrate,and its protein is localized at the plasma membrane after establishment of young seedlings.We found that disruption of CNGC15 results in the loss of the nitrate-induced Ca^(2+) signature(primary nitrate response)and retards root growth,reminiscent of the phenotype observed in the nrt1.1 mutant.We further showed that CNGC15 is an active Ca^(2+)-permeable channel that physically interacts with the NRT1.1 protein in the plasma membrane.Importantly,we discovered that CNGC15-NRT1.1 interaction silences the channel activity of the heterocomplex,which dissociates upon a rise in nitrate levels,leading to reactivation of the CNGC15 channel.The dynamic interactions between CNGC15 and NRT1.1 therefore control the channel activity and Ca^(2+) influx in a nitrate-dependent manner.Our study reveals a new nutrient-sensing mechanism that utilizes a nutrient transceptor-channel complex assembly to couple nutrient status to a specific Ca^(2+) signature.展开更多
The Rad1 gene is evolutionarily conserved from yeast to human.The fission yeast Schizosaccharomyces pombe Rad1 ortholog promotes cell survival against DNA damage and is required for G_(2)/M checkpoint activation.In th...The Rad1 gene is evolutionarily conserved from yeast to human.The fission yeast Schizosaccharomyces pombe Rad1 ortholog promotes cell survival against DNA damage and is required for G_(2)/M checkpoint activation.In this study,mouse embryonic stem(ES)cells with a targeted deletion of Mrad1,the mouse ortholog of this gene,were created to evaluate its function in mammalian cells.Mrad1^(−/−)ES cells were highly sensitive to ultraviolet-light(UV light),hydroxyurea(HU)and gamma rays,and were defective in G_(2)/M as well as S/M checkpoints.These data indicate that Mrad1 is required for repairing DNA lesions induced by UV-light,HU and gamma rays,and for mediating G_(2)/M and S/M checkpoint controls.We further demonstrated that Mrad1 plays an important role in homologous recombination repair(HRR)in ES cells,but a minor HRR role in differentiated mouse cells.展开更多
Grain size is determined by the size and number of cells in the grain.The regulation of grain size is crucial for improving crop yield;however,the genes and molecular mechanisms that control grain size remain elusive....Grain size is determined by the size and number of cells in the grain.The regulation of grain size is crucial for improving crop yield;however,the genes and molecular mechanisms that control grain size remain elusive.Here,we report that a member of the detoxification efflux carrier/Multidrug and Toxic Compound Extrusion(DTX/MATE)family transporters,BIG RICE GRAIN 1(BIRG1),negatively influences grain size in rice(Oryza sativa L.).BIRG1 is highly expressed in reproductive organs and roots.In birg1 grain,the outer parenchyma layer cells of spikelet hulls are larger than in wild-type(WT)grains,but the cell number is unaltered.When expressed in Xenopus laevis oocytes,BIRG1 exhibits chloride efflux activity.Consistent with this role of BIRG1,the birg1 mutant shows reduced tolerance to salt stress at a toxic chloride level.Moreover,grains from birg1 plants contain a higher level of chloride than those of WT plants when grown under normal paddy field conditions,and the roots of birg1 accumulate more chloride than those of WT under saline conditions.Collectively,the data suggest that BIRG1 in rice functions as a chloride efflux transporter that is involved in mediating grain size and salt tolerance by controlling chloride homeostasis.展开更多
基金Acknowledgment We thank the Arabidopsis Biological Resource Center （Ohio State University, Columbus） for providing the Arabidopsis seeds and the editor for was supported by careful reading of the manuscript. This work the National Natural Science Foundation of China （30470879） and Funding Project for Academic Human Resources Development in Institutions of Higher Learning Under the Jurisdiction of Beijing Municipality to He, and National Natural Science Foundation of China （30500288） and Science and Technology Development Program of Beijing Municipal Education Committee grant （KM200610028010） of Beijing Education Committee to Hu.
文摘Chloroplasts are plant-specific organelles that evolved from endosymbiotic cyanobacteria. They divide through binary fission. Selection of the chloroplast division site is pivotal for the symmetric chloroplast division. In E. coli, positioning of the division site at the midpoint of the cell is regulated by dynamic oscillation of the Min system, which includes MinC, MinD and MinE. Homologs of MinD and MinE in plants are involved in chloroplast division. The homolog of MinC still has not been identified in higher plants. However, an FtsZ-like protein, ARC3, was found to be involved in chloroplast division site positioning. Here, we report that chloroplast division site positioning 1 （AtCDP1） is a novel chloroplast division protein involved in chloroplast division site placement in Arabidopsis. AtCDP1 was discovered by screening an Arabidopsis cDNA expression library in bacteria for colonies with a cell division phenotype. AtCDP1 is exclusively expressed in young green tissues in Arabidopsis. Elongated chloroplasts with multiple division sites were observed in the loss-of-function cdpl mutant. Overexpression of AtCDP1 caused a chloroplast division phenotype too. Protein interaction assays suggested that AtCDP1 may mediate the chloroplast division site positioning through the interaction with ARC3. Overall, our results indicate that AtCDP1 is a novel component of the chloroplast division site positioning system, and the working mechanism of this system is different from that of the traditional MinCDE system in prokaryotic cells.
文摘PHYTOCHROME INTERACTING FACTOR3 （PIF3） is an important component in the phytochrome signaling pathway and mediates plant responses to various environmental conditions. We found that PIF3 is involved in the inhibition of root growth of Arabidopsis thaliana seedlings induced by nitric oxide （NO） in light. Overexpression of PIF3 partially alleviated the inhibitory effect of NO on root growth, whereas the pif3-1 mutant displayed enhanced sensitivity to NO in terms of root growth. During phytochrome signaling, the photoreceptor PHYB mediates the degradation of PIF3. We found that the phyB-9 mutant had a similar phenotype to that of PIF3ox in terms of responsiveness to NO. Furthermore, NO treatment promoted the accumulation of PHYB, and thus reduced PIF3 content. Our results further show that the activity of PIF3 is regulated by the DELLA protein RGL3[RGA （repressor of gal-3） LIKE 3]. Therefore, we speculate that PIF3 lies downstream of PHYB and RGL3, and plays an important role in the inhibitory effect of NO on root growth of Arabidopsis seedlings in light.
文摘Sessile plants can adjust their growth and development in response to environmental stimuli.Sunlight(light),is the primary source of energy for all life on the earth,in the long course of phylogenetic evolution,plants have developed a unique relationship with light:they can absorb light energy and convert it into organic matter for use by themselves and others。
基金supported by grants from the Key Program of the National Natural Science Foundation of China(31930010 to L.L.)the General Program of National Natural Science Foundation of China(no.31872170 to L.L.and no.31900234 to C.H.)+2 种基金the National Key Research and Development Program of China(YFD0300102-3 to L.L.)the Capacity Building for Sci-Tech Innovation-Fundamental Scientific Research Funds(19530050165 to L.L.).supported,in part,by a grant from the National Science Foundation(MCB-1714795 to S.L.).
文摘Nitrate-induced Ca^(2+) signaling is crucial for the primary nitrate response in plants.However,the molecular mechanism underlying the generation of the nitrate-specific calcium signature remains unknown.We report here that a cyclic nucleotide-gated channel(CNGC)protein,CNGC15,and the nitrate transceptor(NRT1.1)constitute a molecular switch that controls calcium influx depending on nitrate levels.The expression of CNGC15 is induced by nitrate,and its protein is localized at the plasma membrane after establishment of young seedlings.We found that disruption of CNGC15 results in the loss of the nitrate-induced Ca^(2+) signature(primary nitrate response)and retards root growth,reminiscent of the phenotype observed in the nrt1.1 mutant.We further showed that CNGC15 is an active Ca^(2+)-permeable channel that physically interacts with the NRT1.1 protein in the plasma membrane.Importantly,we discovered that CNGC15-NRT1.1 interaction silences the channel activity of the heterocomplex,which dissociates upon a rise in nitrate levels,leading to reactivation of the CNGC15 channel.The dynamic interactions between CNGC15 and NRT1.1 therefore control the channel activity and Ca^(2+) influx in a nitrate-dependent manner.Our study reveals a new nutrient-sensing mechanism that utilizes a nutrient transceptor-channel complex assembly to couple nutrient status to a specific Ca^(2+) signature.
基金supported by the National Natural Science Foundation of China(Grant No.30900813 to ZSH)the Knowledge Innovation Program of Chinese Academy of Sciences to HH(Grant No.KSCX2-YW-R63).
文摘The Rad1 gene is evolutionarily conserved from yeast to human.The fission yeast Schizosaccharomyces pombe Rad1 ortholog promotes cell survival against DNA damage and is required for G_(2)/M checkpoint activation.In this study,mouse embryonic stem(ES)cells with a targeted deletion of Mrad1,the mouse ortholog of this gene,were created to evaluate its function in mammalian cells.Mrad1^(−/−)ES cells were highly sensitive to ultraviolet-light(UV light),hydroxyurea(HU)and gamma rays,and were defective in G_(2)/M as well as S/M checkpoints.These data indicate that Mrad1 is required for repairing DNA lesions induced by UV-light,HU and gamma rays,and for mediating G_(2)/M and S/M checkpoint controls.We further demonstrated that Mrad1 plays an important role in homologous recombination repair(HRR)in ES cells,but a minor HRR role in differentiated mouse cells.
基金supported by grants from the National Key Research and Development Program of China(YFD0300102-3 to L.G.L.)the General Program of National Natural Science Foundation of China(No.31872170 to L.L.and No.31900234 to C.H.)+1 种基金the Key Program of the National Natural Science Foundation of China(31930010 to L.L.)the Capacity Building for Sci-Tech Innovation-Fundamental Scientific Research Funds(19530050165 to L.L.)。
文摘Grain size is determined by the size and number of cells in the grain.The regulation of grain size is crucial for improving crop yield;however,the genes and molecular mechanisms that control grain size remain elusive.Here,we report that a member of the detoxification efflux carrier/Multidrug and Toxic Compound Extrusion(DTX/MATE)family transporters,BIG RICE GRAIN 1(BIRG1),negatively influences grain size in rice(Oryza sativa L.).BIRG1 is highly expressed in reproductive organs and roots.In birg1 grain,the outer parenchyma layer cells of spikelet hulls are larger than in wild-type(WT)grains,but the cell number is unaltered.When expressed in Xenopus laevis oocytes,BIRG1 exhibits chloride efflux activity.Consistent with this role of BIRG1,the birg1 mutant shows reduced tolerance to salt stress at a toxic chloride level.Moreover,grains from birg1 plants contain a higher level of chloride than those of WT plants when grown under normal paddy field conditions,and the roots of birg1 accumulate more chloride than those of WT under saline conditions.Collectively,the data suggest that BIRG1 in rice functions as a chloride efflux transporter that is involved in mediating grain size and salt tolerance by controlling chloride homeostasis.
