By considering the eigenratio of the Laplacian matrix as the synchronizability measure, this paper presents an efficient method to enhance the synchronizability of undirected and unweighted networks via rewiring. The ...By considering the eigenratio of the Laplacian matrix as the synchronizability measure, this paper presents an efficient method to enhance the synchronizability of undirected and unweighted networks via rewiring. The rewiring method combines the use of tabu search and a local greedy algorithm so that an effective search of solutions can be achieved. As demonstrated in the simulation results, the performance of the proposed approach outperforms the existing methods for a large variety of initial networks, both in terms of speed and quality of solutions.展开更多
Interspecific hybridization is a driving force in evolution and speciation of higher plants. Interspecific hybridization often induces immediate and saltational changes in gene expression, a phenomenon collectively te...Interspecific hybridization is a driving force in evolution and speciation of higher plants. Interspecific hybridization often induces immediate and saltational changes in gene expression, a phenomenon collectively termed ＂transcriptome shock＂. Although transcriptome shock has been reported in various plant and animal taxa, the extent and pattern of shock-induced expression changes are often highly idiosyncratic, and hence entails additional investigations. Here, we produced a set of interspecific F1 triploid hybrid plants between Oryza sativa, ssp. japonica （2n=2x=24, genome AA） and the tetraploid form of O. punctata （2n=4x =48, genome, BBCC）, and conducted RNA-seq transcriptome profiling of the hybrids and their exact parental plants. We analyzed both homeolog expression bias and overall gene expression level difference in the hybrids relative to the in silico ＂hybrids＂ （parental mixtures）. We found that approximately 16% （2,541） of the 16,112 expressed genes in leaf tissue of the F1 hybrids showed nonadditive expression, which were specifically enriched in photosynthesis-related pathways. Interestingly, changes in the maternal homeolog expression, including non-stochastic silencing, were the major causes for altered homeolog expression partitioning in the F1 hybrids. Our findings have provided further insights into the tran- scriptome response to interspecific hybridization and heterosis.展开更多
MEK is a canonical effector of mutant KRAS;however,MEK inhibitors fail to yield satisfactory clinical outcomes in KRAS-mutant cancers.Here,we identified mitochondrial oxidative phosphorylation(OXPHOS)induction as a pr...MEK is a canonical effector of mutant KRAS;however,MEK inhibitors fail to yield satisfactory clinical outcomes in KRAS-mutant cancers.Here,we identified mitochondrial oxidative phosphorylation(OXPHOS)induction as a profound metabolic alteration to confer KRAS-mutant non-small cell lung cancer(NSCLC)resistance to the clinical MEK inhibitor trametinib.Metabolic flux analysis demonstrated that pyruvate metabolism and fatty acid oxidation were markedly enhanced and coordinately powered the OXPHOS system in resistant cells after trametinib treatment,satisfying their energy demand and protecting them from apoptosis.As molecular events in this process,the pyruvate dehydrogenase complex(PDHc)and carnitine palmitoyl transferase IA(CPTIA),two rate-limiting enzymes that control the metabolic flux of pyruvate and palmitic acid to mitochondrial respiration were activated through phosphorylation and transcriptional regulation.Importantly,the co-administration of trametinib and IACS-010759,a clinical mitochondrial complex I inhibitor that blocks OXPHOS,significantly impeded tumor growth and prolonged mouse survival.Overall,our findings reveal that MEK inhibitor therapy creates a metabolic vulnerability in the mitochondria and further develop an effective combinatorial strategy to circumvent MEK inhibitors resistance in KRAS-driven NSCLC.展开更多
Although extensively studied,it is unknown what is the major cellular energy driving tumor metastasis after anti-cancer radiotherapy.Metabolic reprogramming is one of the fundamental hallmarks in carcinogenesis and tu...Although extensively studied,it is unknown what is the major cellular energy driving tumor metastasis after anti-cancer radiotherapy.Metabolic reprogramming is one of the fundamental hallmarks in carcinogenesis and tumor progression featured with the increased glycolysis in solid tumors.However,accumulating evidence indicates that in addition to the rudimentary glycolytic pathway,tumor cells are capable of reactivating mitochondrial OxPHOS under genotoxic stress condition to meet the increasing cellular fuel demand for repairing and surviving anti-cancer radiation.Such dynamic metabolic rewiring may play a key role in cancer therapy resistance and metastasis.Interestingly,data from our group and others have demonstrated that cancer cells can re-activate mitochondrial oxidative respiration to boost an annexing energy to meet the increasing cellular fuel demand for tumor cells surviving genotoxic anti-cancer therapy with metastatic potential.展开更多
Serotonin is a monoamine neurotransmitter synthetized in various populations of brainstem neurons.In the spinal cord,descending serotonergic projections regulate postural muscle tone,locomotion and rhythm and coordina...Serotonin is a monoamine neurotransmitter synthetized in various populations of brainstem neurons.In the spinal cord,descending serotonergic projections regulate postural muscle tone,locomotion and rhythm and coordination of movements via the Central Pattern Generator.Following a spinal cord injury,serotonergic projections to the lumbar spinal cord,where the Central Pattern Generators are located,are interrupted resulting in devastating locomotor impairments and changes in the expression and activation of serotonin and its spinal receptors.The molecular cues that control the precise patterning and targeting of serotonergic inputs onto Central Pattern Generator networks in healthy animals or after injury are still unknown.In our recent research work,we have been particularly interested in Semaphorin7A,which belongs to the Semaphorins family involved in guiding growing axons and controlling plasticity of synaptic connections.In this review,we discuss the role of Semaphorin7A signaling as an important molecular actor that instructs the patterning of serotonin inputs to spinal Central Pattern Generator networks.We show that Semaphorin7A controls the wiring of descending serotonin axons in the spinal cord.Our results reveal that mistargetting of serotonin fibers in the spinal cord is compensated in healthy uninjured Semaphorin7A deficient mice so that their gross locomotion proceeds accurately.We also demonstrate that when the system is challenged with a spinal lesion,the pattern of post-injury serotonin expression is significantly altered in Semaphorin7A deficient mice with specific ectopic targeting of serotonin fibers in the lumbar spinal cord.Compensatory mechanisms in place in uninjured Semaphorin7A deficient mice are lost and injured Semaphorin7A deficient mice exhibit a worsening of their post-injury locomotor abilities.Our findings identify Semaphorin7A as a critical determinant of serotonergic circuit formation in healthy or spinal cord injured mice.展开更多
Rewiring and reprogramming of transcriptional regulation took place during bacterial speciation. The mechanistic alterations among tran- scription factors, cis-regulatory elements and target genes confer bacteria nove...Rewiring and reprogramming of transcriptional regulation took place during bacterial speciation. The mechanistic alterations among tran- scription factors, cis-regulatory elements and target genes confer bacteria novel ability to adapt to stochastic environmental changes. This process is critical to their survival, especially for bacterial pathogens subjected to accelerated evolution. In the past two decades, the investigators not only completed the sequences of numerous bacterial genomes, but also made great progress in understanding the molecular basis of evolution. Here we briefly reviewed the current knowledge on the mechanistic changes among orthologous, paralogous and xenogenic regulatory circuits, which were caused by genetic recombinations such as gene duplication, horizontal gene transfer, transposable elements and different genetic contexts. We also discussed the potential impact of this area on theoretical and applied studies of microbes.展开更多
Cyanobacteria can utilize CO2 or even N2 to produce a variety of high value-added products efficiently.Plastoquinone(PQ)is an important electron carrier in both of the photosynthetic and respiratory electron transport...Cyanobacteria can utilize CO2 or even N2 to produce a variety of high value-added products efficiently.Plastoquinone(PQ)is an important electron carrier in both of the photosynthetic and respiratory electron transport chain.Although the content of PQ,as well as their redox state,have an important effect on physiology and metabolism,there are relatively few studies on the synthesis of PQ and its related metabolic regulation mechanism in photosynthetic microorganisms.In this study,the strategies of overexpression of Geranyl diphosphate:4-hydroxybenzoate geranyltransferase(lepgt)and addition of 4-hydroxybenzoate(4-HB)as the quinone ring precursor were adopted to regulate the biosynthesis of PQ in Synechocystis PCC 6803.Combined with the analysis the photosystem activity,respiration rate and metabolic components,we found the changes of intracellular PQ reprogrammed the metabolism of Synechocystis PCC 6803.The results showed that the overexpression of lepgt reduced PQ content dramatically,by 22.18%.Interestingly,both of the photosynthesis and respiration rate were enhanced.In addition,the intracellular lipid and protein contents were significantly increased.Whereas,the addition of low concentrations of 4-HB enhanced the biosynthesis of PQ,and the intracellular PQ contents were increased by 14.76%-70.86%in different conditions.Addition of 4-HB can regulate the photosystem efficiency and respiration and reprogram the metabolism of Synechocystis PCC 6803 efficiently.In a word,regulating the PQ biosynthesis provided a novel idea for promoting the reprogramming the physiology and metabolism of Synechocystis.展开更多
Resistance to targeted anti-cancer drugs is a complex phenomenon and a major challenge in cancer treatment.It is becoming increasingly evident that a form of acquired drug resistance known as“adaptive resistance”is ...Resistance to targeted anti-cancer drugs is a complex phenomenon and a major challenge in cancer treatment.It is becoming increasingly evident that a form of acquired drug resistance known as“adaptive resistance”is a common cause of treatment failure and patient relapse in many cancers.Unlike classical resistance mechanisms that are acquired via genomic alterations,adaptive resistance is instead driven by non-genomic changes involving rapid and dynamic rewiring of signalling and/or transcriptional networks following therapy,enabled by complex pathway crosstalk and feedback regulation.Such network rewiring allows tumour cells to adapt to the drug treatment,circumvent the initial drug challenge and continue to survive in the presence of the drug.Despite its great clinical importance,adaptive resistance remains largely under-studied and poorly defined.This review is focused on recent findings which provide new insights into the mechanisms underlying adaptive resistance in breast cancer,highlighting how breast tumour cells rewire intracellular signalling pathways to overcome the stress of initial targeted therapy.In particular,we investigate adaptive resistance to targeted inhibition of two major oncogenic signalling axes frequently dysregulated in breast cancer,the PI3K-AKT-mTOR and RAS-MAPK signalling pathways;and discuss potential combination treatment strategies that overcome such resistance.In addition,we highlight application of quantitative and computational modelling as a novel integrative and powerful approach to gain network-level understanding of network rewiring,and rationally identify and prioritise effective drug combinations.展开更多
Over the last few years,the interplay between contagion dynamics of social influences(e.g.,human awareness,risk perception,and information dissemination)and biological infections has been extensively investigated with...Over the last few years,the interplay between contagion dynamics of social influences(e.g.,human awareness,risk perception,and information dissemination)and biological infections has been extensively investigated within the framework of multiplex networks.The vast majority of existing multiplex network spreading models typically resort to heterogeneous mean-field approximation and microscopic Markov chain approaches.Such approaches usually manifest richer dynamical properties on multiplex networks than those on simplex networks;however,they fall short of a subtle analysis of the variations in connections between nodes of the network and fail to account for the adaptive behavioral changes among individuals in response to epidemic outbreaks.To transcend these limitations,in this paper we develop a highly integrated effective degree approach to modeling epidemic and awareness spreading processes on multiplex networks coupled with awareness-dependent adaptive rewiring.This approach keeps track of the number of nearest neighbors in each state of an individual;consequently,it allows for the integration of changes in local contacts into the multiplex network model.We derive a formula for the threshold condition of contagion outbreak.Also,we provide a lower bound for the threshold parameter to indicate the effect of adaptive rewiring.The threshold analysis is confirmed by extensive simulations.Our results show that awareness-dependent link rewiring plays an important role in enhancing the transmission threshold as well as lowering the epidemic prevalence.Moreover,it is revealed that intensified awareness diffusion in conjunction with enhanced link rewiring makes a greater contribution to disease prevention and control.In addition,the critical phenomenon is observed in the dependence of the epidemic threshold on the awareness diffusion rate,supporting the metacritical point previously reported in literature.This work may shed light on understanding of the interplay between epidemic dynamics and social contagion on adaptiv展开更多
Aims Plant-pollinator interaction networks are dynamic entities,and seasonal variation in plant phenology can reshape their structure on both short and long timescales.However,such seasonal dynamics are rarely conside...Aims Plant-pollinator interaction networks are dynamic entities,and seasonal variation in plant phenology can reshape their structure on both short and long timescales.However,such seasonal dynamics are rarely considered,especially for oceanic island pollination networks.Here,we assess changes in the temporal dynamics of plant-pollinator interactions in response to seasonal variation in floral resource richness in oceanic island communities.Methods We evaluated seasonal variations of pollination networks in the Yongxing Island community.Four temporal qualitative pollination networks were analyzed using plant-pollinator interaction data of the four seasons.We collected data on plant-pollinator interactions during two consecutive months in each of the four seasons.Four network-level indices were calculated to characterize the overall structure of the networks.Statistical analyses of community dissimilarity were used to compare this community across four seasons to explore the underlying factors driving these patterns.We also evaluated the temporal variation in two species-level indices of plant and pollinator functional groups.Important Findings Both network-level specialization and modularity showed a significantly opposite trend compared with plant species richness across four seasons.Increased numbers of plant species might promote greater competition among pollinators,leading to increased niche overlap and causing decreased specialization and modularity and vice versa.Further analyses suggested that the season-to-season turnover of interactions was dominated by interaction rewiring.Thus,the seasonal changes in niche overlap among pollinators lead to interaction rewiring,which drives interaction turnover in this community.Hawkmoths had higher values of specialization and Apidae had higher values of species strength compared with other pollinator functional groups.These findings should be considered when exploring plant-pollinator interactions in ecosystems of isolated oceanic islands and in other ecosystems.展开更多
基金Project supported by the grant from City University of Hong Kong (Grant No. 7008105)
文摘By considering the eigenratio of the Laplacian matrix as the synchronizability measure, this paper presents an efficient method to enhance the synchronizability of undirected and unweighted networks via rewiring. The rewiring method combines the use of tabu search and a local greedy algorithm so that an effective search of solutions can be achieved. As demonstrated in the simulation results, the performance of the proposed approach outperforms the existing methods for a large variety of initial networks, both in terms of speed and quality of solutions.
基金supported by the National Natural Science Foundation of China (NSFC#30990243)the State Key Basic Research and Development Plan of China (2013CBA01404)+1 种基金the Program for Introducing Talents to Universities (#B07017)a Graduate Student Innovation Fund (12SSXT130)
文摘Interspecific hybridization is a driving force in evolution and speciation of higher plants. Interspecific hybridization often induces immediate and saltational changes in gene expression, a phenomenon collectively termed ＂transcriptome shock＂. Although transcriptome shock has been reported in various plant and animal taxa, the extent and pattern of shock-induced expression changes are often highly idiosyncratic, and hence entails additional investigations. Here, we produced a set of interspecific F1 triploid hybrid plants between Oryza sativa, ssp. japonica （2n=2x=24, genome AA） and the tetraploid form of O. punctata （2n=4x =48, genome, BBCC）, and conducted RNA-seq transcriptome profiling of the hybrids and their exact parental plants. We analyzed both homeolog expression bias and overall gene expression level difference in the hybrids relative to the in silico ＂hybrids＂ （parental mixtures）. We found that approximately 16% （2,541） of the 16,112 expressed genes in leaf tissue of the F1 hybrids showed nonadditive expression, which were specifically enriched in photosynthesis-related pathways. Interestingly, changes in the maternal homeolog expression, including non-stochastic silencing, were the major causes for altered homeolog expression partitioning in the F1 hybrids. Our findings have provided further insights into the tran- scriptome response to interspecific hybridization and heterosis.
基金sponsored by the National Natural Science Foundation of China(82122045,82073073,81874207,and 81872418)Innovative Research Team of High-level Local Universities in Shanghai(SHSMU-ZDCX20210802,China)+4 种基金MOE Key Laboratory of Biosystems Homeostasis&Protection(Zhejiang University,China)Science and Technology Commission of Shanghai Municipality(21S11902000,China)Jointed PI Program from Shanghai Changning Maternity and Infant Health Hospital(11300-412311-20033,China)ECNU Construction Fund of Innovation and Entrepreneurship Laboratory(44400-20201-532300/021,China)the ECNU multifunctional platform for innovation(011 and 004,China).
文摘MEK is a canonical effector of mutant KRAS;however,MEK inhibitors fail to yield satisfactory clinical outcomes in KRAS-mutant cancers.Here,we identified mitochondrial oxidative phosphorylation(OXPHOS)induction as a profound metabolic alteration to confer KRAS-mutant non-small cell lung cancer(NSCLC)resistance to the clinical MEK inhibitor trametinib.Metabolic flux analysis demonstrated that pyruvate metabolism and fatty acid oxidation were markedly enhanced and coordinately powered the OXPHOS system in resistant cells after trametinib treatment,satisfying their energy demand and protecting them from apoptosis.As molecular events in this process,the pyruvate dehydrogenase complex(PDHc)and carnitine palmitoyl transferase IA(CPTIA),two rate-limiting enzymes that control the metabolic flux of pyruvate and palmitic acid to mitochondrial respiration were activated through phosphorylation and transcriptional regulation.Importantly,the co-administration of trametinib and IACS-010759,a clinical mitochondrial complex I inhibitor that blocks OXPHOS,significantly impeded tumor growth and prolonged mouse survival.Overall,our findings reveal that MEK inhibitor therapy creates a metabolic vulnerability in the mitochondria and further develop an effective combinatorial strategy to circumvent MEK inhibitors resistance in KRAS-driven NSCLC.
基金J.J.L is supported by a US National Institutes of Health(NIH)grant(RO1 CA213830).
文摘Although extensively studied,it is unknown what is the major cellular energy driving tumor metastasis after anti-cancer radiotherapy.Metabolic reprogramming is one of the fundamental hallmarks in carcinogenesis and tumor progression featured with the increased glycolysis in solid tumors.However,accumulating evidence indicates that in addition to the rudimentary glycolytic pathway,tumor cells are capable of reactivating mitochondrial OxPHOS under genotoxic stress condition to meet the increasing cellular fuel demand for repairing and surviving anti-cancer radiation.Such dynamic metabolic rewiring may play a key role in cancer therapy resistance and metastasis.Interestingly,data from our group and others have demonstrated that cancer cells can re-activate mitochondrial oxidative respiration to boost an annexing energy to meet the increasing cellular fuel demand for tumor cells surviving genotoxic anti-cancer therapy with metastatic potential.
基金Work in FMB.’s lab is supported by grants from the Deutsche Forschungsgemeinschaft(DFG,SFB 870 and CRC 274)by the Munich Center for Neurosciences(MCN)and the International Foundation for Research in Paraplegia(IRP)(to FMB)supported by the Munich Center for Systems Neurology(DFG,Sy Nergy,EXC 2145/ID 390857198)。
文摘Serotonin is a monoamine neurotransmitter synthetized in various populations of brainstem neurons.In the spinal cord,descending serotonergic projections regulate postural muscle tone,locomotion and rhythm and coordination of movements via the Central Pattern Generator.Following a spinal cord injury,serotonergic projections to the lumbar spinal cord,where the Central Pattern Generators are located,are interrupted resulting in devastating locomotor impairments and changes in the expression and activation of serotonin and its spinal receptors.The molecular cues that control the precise patterning and targeting of serotonergic inputs onto Central Pattern Generator networks in healthy animals or after injury are still unknown.In our recent research work,we have been particularly interested in Semaphorin7A,which belongs to the Semaphorins family involved in guiding growing axons and controlling plasticity of synaptic connections.In this review,we discuss the role of Semaphorin7A signaling as an important molecular actor that instructs the patterning of serotonin inputs to spinal Central Pattern Generator networks.We show that Semaphorin7A controls the wiring of descending serotonin axons in the spinal cord.Our results reveal that mistargetting of serotonin fibers in the spinal cord is compensated in healthy uninjured Semaphorin7A deficient mice so that their gross locomotion proceeds accurately.We also demonstrate that when the system is challenged with a spinal lesion,the pattern of post-injury serotonin expression is significantly altered in Semaphorin7A deficient mice with specific ectopic targeting of serotonin fibers in the lumbar spinal cord.Compensatory mechanisms in place in uninjured Semaphorin7A deficient mice are lost and injured Semaphorin7A deficient mice exhibit a worsening of their post-injury locomotor abilities.Our findings identify Semaphorin7A as a critical determinant of serotonergic circuit formation in healthy or spinal cord injured mice.
基金supported by the National Basic Research Program(No.2011CB 100700)of the Ministry of Science and Technology of Chinathe National Natural Science Foundation of China(Nos.30771401 and 31070081)the Startup Fund from the Institute of Microbiology,Chinese Academy of Sciences
文摘Rewiring and reprogramming of transcriptional regulation took place during bacterial speciation. The mechanistic alterations among tran- scription factors, cis-regulatory elements and target genes confer bacteria novel ability to adapt to stochastic environmental changes. This process is critical to their survival, especially for bacterial pathogens subjected to accelerated evolution. In the past two decades, the investigators not only completed the sequences of numerous bacterial genomes, but also made great progress in understanding the molecular basis of evolution. Here we briefly reviewed the current knowledge on the mechanistic changes among orthologous, paralogous and xenogenic regulatory circuits, which were caused by genetic recombinations such as gene duplication, horizontal gene transfer, transposable elements and different genetic contexts. We also discussed the potential impact of this area on theoretical and applied studies of microbes.
基金This work was sponsored by National Key Research and Development Project of China 2019YFA0906300 and 2020YFA0907304National Natural Science Foundation of China 21776083+3 种基金the Fok Ying Tong Education Foundation 161017Natural Science Foundation of Shandong Province ZR2019ZD17Natural Science Foundation of Shanghai 21ZR1416400 and 19ZR1472700the Fundamental Research Funds for the Central Universities 22221818014,Funding Project of the State Key Laboratory of Bioreactor Engineering.
文摘Cyanobacteria can utilize CO2 or even N2 to produce a variety of high value-added products efficiently.Plastoquinone(PQ)is an important electron carrier in both of the photosynthetic and respiratory electron transport chain.Although the content of PQ,as well as their redox state,have an important effect on physiology and metabolism,there are relatively few studies on the synthesis of PQ and its related metabolic regulation mechanism in photosynthetic microorganisms.In this study,the strategies of overexpression of Geranyl diphosphate:4-hydroxybenzoate geranyltransferase(lepgt)and addition of 4-hydroxybenzoate(4-HB)as the quinone ring precursor were adopted to regulate the biosynthesis of PQ in Synechocystis PCC 6803.Combined with the analysis the photosystem activity,respiration rate and metabolic components,we found the changes of intracellular PQ reprogrammed the metabolism of Synechocystis PCC 6803.The results showed that the overexpression of lepgt reduced PQ content dramatically,by 22.18%.Interestingly,both of the photosynthesis and respiration rate were enhanced.In addition,the intracellular lipid and protein contents were significantly increased.Whereas,the addition of low concentrations of 4-HB enhanced the biosynthesis of PQ,and the intracellular PQ contents were increased by 14.76%-70.86%in different conditions.Addition of 4-HB can regulate the photosystem efficiency and respiration and reprogram the metabolism of Synechocystis PCC 6803 efficiently.In a word,regulating the PQ biosynthesis provided a novel idea for promoting the reprogramming the physiology and metabolism of Synechocystis.
基金This work was supported by the Victorian Cancer Agency Mid-Career Research Fellowship(MCRF18026)the Cancer Council Victoria Grant in Aid,Ref.No.1123892CC awarded to Lan K Nguyen(Nguyen LK).
文摘Resistance to targeted anti-cancer drugs is a complex phenomenon and a major challenge in cancer treatment.It is becoming increasingly evident that a form of acquired drug resistance known as“adaptive resistance”is a common cause of treatment failure and patient relapse in many cancers.Unlike classical resistance mechanisms that are acquired via genomic alterations,adaptive resistance is instead driven by non-genomic changes involving rapid and dynamic rewiring of signalling and/or transcriptional networks following therapy,enabled by complex pathway crosstalk and feedback regulation.Such network rewiring allows tumour cells to adapt to the drug treatment,circumvent the initial drug challenge and continue to survive in the presence of the drug.Despite its great clinical importance,adaptive resistance remains largely under-studied and poorly defined.This review is focused on recent findings which provide new insights into the mechanisms underlying adaptive resistance in breast cancer,highlighting how breast tumour cells rewire intracellular signalling pathways to overcome the stress of initial targeted therapy.In particular,we investigate adaptive resistance to targeted inhibition of two major oncogenic signalling axes frequently dysregulated in breast cancer,the PI3K-AKT-mTOR and RAS-MAPK signalling pathways;and discuss potential combination treatment strategies that overcome such resistance.In addition,we highlight application of quantitative and computational modelling as a novel integrative and powerful approach to gain network-level understanding of network rewiring,and rationally identify and prioritise effective drug combinations.
基金the National Natural Science Foundation of China(Grant Nos.11601294 and 61873154),Shanxi Scholarship Council of China(Grant No.2016-011)the Shanxi Province Science Foundation for Youths(Grant Nos.201601D021012,201801D221011,201901D211159,201801D221007 and 201801D221003)the 1331 Engineering Project of Shanxi Province,China.
文摘Over the last few years,the interplay between contagion dynamics of social influences(e.g.,human awareness,risk perception,and information dissemination)and biological infections has been extensively investigated within the framework of multiplex networks.The vast majority of existing multiplex network spreading models typically resort to heterogeneous mean-field approximation and microscopic Markov chain approaches.Such approaches usually manifest richer dynamical properties on multiplex networks than those on simplex networks;however,they fall short of a subtle analysis of the variations in connections between nodes of the network and fail to account for the adaptive behavioral changes among individuals in response to epidemic outbreaks.To transcend these limitations,in this paper we develop a highly integrated effective degree approach to modeling epidemic and awareness spreading processes on multiplex networks coupled with awareness-dependent adaptive rewiring.This approach keeps track of the number of nearest neighbors in each state of an individual;consequently,it allows for the integration of changes in local contacts into the multiplex network model.We derive a formula for the threshold condition of contagion outbreak.Also,we provide a lower bound for the threshold parameter to indicate the effect of adaptive rewiring.The threshold analysis is confirmed by extensive simulations.Our results show that awareness-dependent link rewiring plays an important role in enhancing the transmission threshold as well as lowering the epidemic prevalence.Moreover,it is revealed that intensified awareness diffusion in conjunction with enhanced link rewiring makes a greater contribution to disease prevention and control.In addition,the critical phenomenon is observed in the dependence of the epidemic threshold on the awareness diffusion rate,supporting the metacritical point previously reported in literature.This work may shed light on understanding of the interplay between epidemic dynamics and social contagion on adaptiv
基金supported by the National Natural Science Foundation of China(grant no.31800447)the Chinese Academy of Sciences(grant no.XDA13020504)+1 种基金the Natural Science Foundation of Guangdong Province(grant no.2018A030310385)the National Natural Science Foundation of China(grant no.U1701246).
文摘Aims Plant-pollinator interaction networks are dynamic entities,and seasonal variation in plant phenology can reshape their structure on both short and long timescales.However,such seasonal dynamics are rarely considered,especially for oceanic island pollination networks.Here,we assess changes in the temporal dynamics of plant-pollinator interactions in response to seasonal variation in floral resource richness in oceanic island communities.Methods We evaluated seasonal variations of pollination networks in the Yongxing Island community.Four temporal qualitative pollination networks were analyzed using plant-pollinator interaction data of the four seasons.We collected data on plant-pollinator interactions during two consecutive months in each of the four seasons.Four network-level indices were calculated to characterize the overall structure of the networks.Statistical analyses of community dissimilarity were used to compare this community across four seasons to explore the underlying factors driving these patterns.We also evaluated the temporal variation in two species-level indices of plant and pollinator functional groups.Important Findings Both network-level specialization and modularity showed a significantly opposite trend compared with plant species richness across four seasons.Increased numbers of plant species might promote greater competition among pollinators,leading to increased niche overlap and causing decreased specialization and modularity and vice versa.Further analyses suggested that the season-to-season turnover of interactions was dominated by interaction rewiring.Thus,the seasonal changes in niche overlap among pollinators lead to interaction rewiring,which drives interaction turnover in this community.Hawkmoths had higher values of specialization and Apidae had higher values of species strength compared with other pollinator functional groups.These findings should be considered when exploring plant-pollinator interactions in ecosystems of isolated oceanic islands and in other ecosystems.
