Emodin (1,3,8-trihydroxy-6-methylanthraquinone) could enhance the sensitivity of tumor cells to arsenic trioxide(As2O3)–induced apoptosis via generation of ROS, but the molecular mechanism has not been elucidated. He...Emodin (1,3,8-trihydroxy-6-methylanthraquinone) could enhance the sensitivity of tumor cells to arsenic trioxide(As2O3)–induced apoptosis via generation of ROS, but the molecular mechanism has not been elucidated. Here, wecarried out cDNA microarray-based global transcription profiling of HeLa cells in response to As2O3/emodin cotreatment,comparing with As2O3–only treatment. The results showed that the expression of a number of genes was substantiallyaltered at two time points. These genes are involved in different aspects of cell function. In addition to redox regulationand apoptosis, ROS affect genes encoding proteins associated with cell signaling, organelle functions, cell cycle,cytoskeleton, etc. These data suggest that based on the cytotoxicity of As2O3, emodin mobilize every genomic resourcethrough which the As2O3–induced apoptosis is facilitated.展开更多
Intracellular reactive oxygen species(ROS)are known to regulate apoptosis.Activation of caspase-9,the initial caspase in the mitochondrial apoptotic cascade,is closely associated with ROS,but it is unclear whether ROS...Intracellular reactive oxygen species(ROS)are known to regulate apoptosis.Activation of caspase-9,the initial caspase in the mitochondrial apoptotic cascade,is closely associated with ROS,but it is unclear whether ROS regulate caspase-9 via direct oxidative modification.The present study aims to elucidate the molecular mechanisms by which ROS mediate caspase-9 activation.Our results show that the cellular oxidative state facilitates caspase-9 activation.Hydrogen peroxide treatment causes the activation of caspase-9 and apoptosis,and promotes an interac-tion between easpase-9 and apoptotic protease-activating factor 1(Apaf-1)via disulfide formation.In addition,in an in vitro mitochondria-free system,the thiol-oxidant diamide promotes auto-cleavage of caspase-9 and the caspase-9/Apaf-1 interaction by facilitating the formation of disulfide-linked complexes.Finally,a point mutation at C403 of caspase-9 impairs both H2O2-promoted caspase-9 activation and interaction with Apaf-1 through the abolition of disulfide formation.The association between cytochrome c and the C403S mutant is significantly weaker than that between cytochrome c and wild-type caspase-9,indicating that oxidative modification of caspase-9 contributes to apoptosome formation under oxidative stress.Taken together,oxidative modification of caspase-9 by ROS can medi-ate its interaction with Apaf-1,and can thus promote its auto-cleavage and activation.This mechanism may facilitate apoptosome formation and caspase-9 activation under oxidative stress.展开更多
Understanding how plant species richness influences the diversity of herbivorous and predatory/parasitic arthropods is central to community ecology.We explore the effects of crop species richness on the diversity of p...Understanding how plant species richness influences the diversity of herbivorous and predatory/parasitic arthropods is central to community ecology.We explore the effects of crop species richness on the diversity of pest insects and their natural enemies.Using data from a four-year experiment with five levels of crop species richness,we found that crop species richness significantly affected the pest species richness,but there were no significant effects on richness of the pests’natural enemies.In contrast,the species richness of pest insects significantly affected their natural enemies.These findings suggest a cascade effect where trophic interactions are strong between adjacent trophic levels,while the interactions between connected but nonadjacent trophic levels are weakened by the intermediate trophic level.High crop species richness resulted in a more stable arthropod community compared with communities in monoculture crops.Our results highlight the complicated cross-trophic interactions and the crucial role of crop diversity in the food webs of agro-ecosystems.展开更多
基金This study was supported by grants from National Natural Science Foundation of China(No.30170475)Shanghai Municipal Education Commission(No.zdxk2001).
文摘Emodin (1,3,8-trihydroxy-6-methylanthraquinone) could enhance the sensitivity of tumor cells to arsenic trioxide(As2O3)–induced apoptosis via generation of ROS, but the molecular mechanism has not been elucidated. Here, wecarried out cDNA microarray-based global transcription profiling of HeLa cells in response to As2O3/emodin cotreatment,comparing with As2O3–only treatment. The results showed that the expression of a number of genes was substantiallyaltered at two time points. These genes are involved in different aspects of cell function. In addition to redox regulationand apoptosis, ROS affect genes encoding proteins associated with cell signaling, organelle functions, cell cycle,cytoskeleton, etc. These data suggest that based on the cytotoxicity of As2O3, emodin mobilize every genomic resourcethrough which the As2O3–induced apoptosis is facilitated.
文摘Intracellular reactive oxygen species(ROS)are known to regulate apoptosis.Activation of caspase-9,the initial caspase in the mitochondrial apoptotic cascade,is closely associated with ROS,but it is unclear whether ROS regulate caspase-9 via direct oxidative modification.The present study aims to elucidate the molecular mechanisms by which ROS mediate caspase-9 activation.Our results show that the cellular oxidative state facilitates caspase-9 activation.Hydrogen peroxide treatment causes the activation of caspase-9 and apoptosis,and promotes an interac-tion between easpase-9 and apoptotic protease-activating factor 1(Apaf-1)via disulfide formation.In addition,in an in vitro mitochondria-free system,the thiol-oxidant diamide promotes auto-cleavage of caspase-9 and the caspase-9/Apaf-1 interaction by facilitating the formation of disulfide-linked complexes.Finally,a point mutation at C403 of caspase-9 impairs both H2O2-promoted caspase-9 activation and interaction with Apaf-1 through the abolition of disulfide formation.The association between cytochrome c and the C403S mutant is significantly weaker than that between cytochrome c and wild-type caspase-9,indicating that oxidative modification of caspase-9 contributes to apoptosome formation under oxidative stress.Taken together,oxidative modification of caspase-9 by ROS can medi-ate its interaction with Apaf-1,and can thus promote its auto-cleavage and activation.This mechanism may facilitate apoptosome formation and caspase-9 activation under oxidative stress.
基金supported by the National Natural Science Foundation of China (31030012)the National Key Technology Research & Development Program,China (2013CB127604)+2 种基金the Special Fund for Agro-scientific Research in the Public Interest,China (201103012)support from the National Research Foundation,South Africa (76912 and 81825)supported by the University of California Agricultural Experiment Station,Riverside,CA,USA
文摘Understanding how plant species richness influences the diversity of herbivorous and predatory/parasitic arthropods is central to community ecology.We explore the effects of crop species richness on the diversity of pest insects and their natural enemies.Using data from a four-year experiment with five levels of crop species richness,we found that crop species richness significantly affected the pest species richness,but there were no significant effects on richness of the pests’natural enemies.In contrast,the species richness of pest insects significantly affected their natural enemies.These findings suggest a cascade effect where trophic interactions are strong between adjacent trophic levels,while the interactions between connected but nonadjacent trophic levels are weakened by the intermediate trophic level.High crop species richness resulted in a more stable arthropod community compared with communities in monoculture crops.Our results highlight the complicated cross-trophic interactions and the crucial role of crop diversity in the food webs of agro-ecosystems.
