Abrupt changes in radiolarian composition are discovered over the last 600 and 120 ka B. P. based on quantitative analyses of radiolarians in ~ 17957 - 2 of the southern South China Sea. The distinct changes at 600 ka...Abrupt changes in radiolarian composition are discovered over the last 600 and 120 ka B. P. based on quantitative analyses of radiolarians in ~ 17957 - 2 of the southern South China Sea. The distinct changes at 600 ka B. P. could correspond to the onset of the 100 ka cycle during the glacial and interglacial periods. This abrupt change in the 100 ka cyclicity at 600 ka B. P. occurred also in the magnetic susceptibility signal that is obtained from and paleosol sequences of the China Loss Plateau. The larger amplitude and stronger cyclicity in the susceptibility signal after 600 ka B. P. reflect the prominent change in the intensity of the monsoon, induced by an enhancement of the momsoon circula- tion. Stronger seasonality during the glacial period in the South China Sea, resulted from strengthening of winter monsoon, might lead to the changes in the radiolarian composition at 600 and 120 ka B. P. It can be suggested that only species adapted to a broader temperature range might have been able to live in this environment. Therefore, the abrupt changes in radiolarian composition at 600 and 120 ka B. P. could be attributed to the stronger so differences between summer and winter that were caused by the striking change in the intensity of the monsoon circulation.展开更多
The nucleotide-binding and leucine-rich repeat(NLR)proteins comprise a major class of intracellular immune receptors that are capable of detecting pathogen-derived molecules and activating immunity and cell death in p...The nucleotide-binding and leucine-rich repeat(NLR)proteins comprise a major class of intracellular immune receptors that are capable of detecting pathogen-derived molecules and activating immunity and cell death in plants.The activity of some NLRs,particularly the Toll-like/interleukin-1 receptor(TIR)type,is highly correlated with their nucleocytoplasmic distribution.However,whether and how the nucleocytoplasmic homeostasis of NLRs is coordinated through a bidirectional nuclear shuttling mechanism remains unclear.Here,we identified a nuclear transport receptor,KA120,which is capable of affecting the nucleocytoplasmic distribution of an NLR protein and is essential in preventing its autoactivation.We showed that the ka120 mutant displays an autoimmune phenotype and NLR-induced transcriptome features.Through a targeted genetic screen using an artificial NLR microRNA library,we identified the TIR-NLR gene SNC1 as a genetic interactor of KA120.Loss-of-function snc1 mutations as well as compromising SNC1 protein activities all substantially suppressed ka120-induced autoimmune activation,and the enhanced SNC1 activity upon loss of KA120 functionappeared to occur at the protein level.Overexpression of KA120 efficiently repressed SNC1 activity and led to a nearly complete suppression of the autoimmune phenotype caused by the gain-of-function snc1-1 mutation or SNC1 overexpression in transgenic plants.Further florescence imaging analysis indicated that SNC1 undergoes altered nucleocytoplasmic distribution with significantly reduced nuclear signal when KA120 is constitutively expressed,supporting a role of KA120 in coordinating SNC1 nuclear abundance and activity.Consistently,compromising the SNC1 nuclear level by disrupting the nuclear pore complex could also partially rescue ka120-induced autoimmunity.Collectively,our study demonstrates that KA120 is essential to avoid autoimmune activation in the absence of pathogens and is required to constrain the nuclear activity of SNC1,possibly through coordinating SNC1 nucleocytoplasmic homeostasis as a potential mechanism.展开更多
基金This project was supported by the National Natural Science Foundation of China under contract! Nos 49946011 and 49999560 by
文摘Abrupt changes in radiolarian composition are discovered over the last 600 and 120 ka B. P. based on quantitative analyses of radiolarians in ~ 17957 - 2 of the southern South China Sea. The distinct changes at 600 ka B. P. could correspond to the onset of the 100 ka cycle during the glacial and interglacial periods. This abrupt change in the 100 ka cyclicity at 600 ka B. P. occurred also in the magnetic susceptibility signal that is obtained from and paleosol sequences of the China Loss Plateau. The larger amplitude and stronger cyclicity in the susceptibility signal after 600 ka B. P. reflect the prominent change in the intensity of the monsoon, induced by an enhancement of the momsoon circula- tion. Stronger seasonality during the glacial period in the South China Sea, resulted from strengthening of winter monsoon, might lead to the changes in the radiolarian composition at 600 and 120 ka B. P. It can be suggested that only species adapted to a broader temperature range might have been able to live in this environment. Therefore, the abrupt changes in radiolarian composition at 600 and 120 ka B. P. could be attributed to the stronger so differences between summer and winter that were caused by the striking change in the intensity of the monsoon circulation.
基金X.Shen and X.Shi were supported by Tsinghua-Peking Joint Center tor Life SciencesThis project was supported by the USDA National Institute of Food and Agriculture(HATCH project CA-B-PLB-0243-H)+1 种基金the National Science Foundation(grant MCB-2049931)startup funds from Inno-vative Genomics Institute and University of California Berkeley.
文摘The nucleotide-binding and leucine-rich repeat(NLR)proteins comprise a major class of intracellular immune receptors that are capable of detecting pathogen-derived molecules and activating immunity and cell death in plants.The activity of some NLRs,particularly the Toll-like/interleukin-1 receptor(TIR)type,is highly correlated with their nucleocytoplasmic distribution.However,whether and how the nucleocytoplasmic homeostasis of NLRs is coordinated through a bidirectional nuclear shuttling mechanism remains unclear.Here,we identified a nuclear transport receptor,KA120,which is capable of affecting the nucleocytoplasmic distribution of an NLR protein and is essential in preventing its autoactivation.We showed that the ka120 mutant displays an autoimmune phenotype and NLR-induced transcriptome features.Through a targeted genetic screen using an artificial NLR microRNA library,we identified the TIR-NLR gene SNC1 as a genetic interactor of KA120.Loss-of-function snc1 mutations as well as compromising SNC1 protein activities all substantially suppressed ka120-induced autoimmune activation,and the enhanced SNC1 activity upon loss of KA120 functionappeared to occur at the protein level.Overexpression of KA120 efficiently repressed SNC1 activity and led to a nearly complete suppression of the autoimmune phenotype caused by the gain-of-function snc1-1 mutation or SNC1 overexpression in transgenic plants.Further florescence imaging analysis indicated that SNC1 undergoes altered nucleocytoplasmic distribution with significantly reduced nuclear signal when KA120 is constitutively expressed,supporting a role of KA120 in coordinating SNC1 nuclear abundance and activity.Consistently,compromising the SNC1 nuclear level by disrupting the nuclear pore complex could also partially rescue ka120-induced autoimmunity.Collectively,our study demonstrates that KA120 is essential to avoid autoimmune activation in the absence of pathogens and is required to constrain the nuclear activity of SNC1,possibly through coordinating SNC1 nucleocytoplasmic homeostasis as a potential mechanism.
