Plant architecture strongly influences rice grain yield.We report the cloning and characterization of the LTA1 gene,which simultaneously controls tiller angle and yield of rice.LTA1 encodes a chloroplastlocalized prot...Plant architecture strongly influences rice grain yield.We report the cloning and characterization of the LTA1 gene,which simultaneously controls tiller angle and yield of rice.LTA1 encodes a chloroplastlocalized protein with a conserved YbaB DNA-binding domain,and is highly expressed in photosynthetic tissues including leaves and leaf sheaths.Disrupting the function of LTA1 leads to large tiller angle and yield reduction of rice.LTA1 affects the gravity response by mediating the distribution of endogenous auxin,thereby regulating the tiller angle.An lta1 mutant showed abnormal chloroplast development and decreased chlorophyll content and photosynthetic rate,in turn leading to reduction of rice yield.Our findings shed light on the genetic basis of tiller angle and provide a potential gene resource for the improvement of plant architecture and rice yield.展开更多
Increasing evidence has revealed that abscisic acid （ABA） negatively modulates ethylene biosynthesis, although the underlying mechanism remains unclear. To identify the factors involved, we conducted a screen for AB...Increasing evidence has revealed that abscisic acid （ABA） negatively modulates ethylene biosynthesis, although the underlying mechanism remains unclear. To identify the factors involved, we conducted a screen for ABA-insensitive mutants with altered ethylene production in Arabidopsis. A dominant allele of ABI4, abi4-152, which produces a putative protein with a 16-amino-acid truncation at the C-terminus of ABI4, reduces ethylene production. By contrast, two recessive knockout alleles of ABI4, abi4-102 and abi4-103, result in increased ethylene evolution, indicating that ABI4 negatively regulates ethylene produc- tion. Further analyses showed that expression of the ethylene biosynthesis genes ACS4, ACSS, and AC02 was significantly decreased in abi4-152 but increased in the knockout mutants, with partial dependence on ABA. Chromatin immunoprecipitation-quantitative PCR assays showed that ABI4 directly binds the pro- moters of these ethylene biosynthesis genes and that ABA enhances this interaction. A fusion protein containing the truncated ABI4-152 peptide accumulated to higher levels than its full-length counterpart in transgenic plants, suggesting that ABI4 is destabilized by its C terminus. Therefore, our results demon- strate that ABA negatively regulates ethylene production through ABI4-mediated transcriptional repression of the ethylene biosynthesis genes ACS4 and ACS8 in Arabidopsis.展开更多
Type 2 diabetes mellitus(T2DM)and Alzheimer's disease(AD)share several common pathophysiological features.Rare variants of triggering receptor expressed on myeloid cells 2(TREM2)increase the risk of developing AD,...Type 2 diabetes mellitus(T2DM)and Alzheimer's disease(AD)share several common pathophysiological features.Rare variants of triggering receptor expressed on myeloid cells 2(TREM2)increase the risk of developing AD,suggesting the involvement of TREM2 and innate immunity in AD development.It is still unknown whether TREM2 is related to cognitive impairment in T2DM.Here,we investigated the effects of the hippocampal overexpression of TREM2 on cognitive in long-term high-fat diet(HFD)-fed mice.Male C57BL/6J mice were maintained on HFD for 50 weeks.TREM2 was overexpressed in the hippocampus 36 weeks after HFD feeding using adeno-associated virus vector(AAV)-mediated gene delivery.The results showed that the HFD feeding induced rapid and persistent weight gain,glucose intolerance and significant impairments in learning and memory.Compared with AAV-con,AAV-TREM2 significantly ameliorated cognitive impairment without altering body weight and glucose homeostasis in HFD mice.The overexpression of TREM2 upregulated the synaptic proteins spinophilin,PSD95 and synaptophysin,suggesting the improvement in synaptic transmission.Dendritic complexity and spine density in the CA1 region were rescued after TREM2 overexpression.Furthermore,TREM2 markedly increased the number of iba-1/Arg-1-positive microglia in the hippocampus,suppressed neuroinflammation and microglial activation.In sum,hippocampal TREM2 plays an important role in improving HFD-induced cognitive dysfunction and promoting microglial polarization towards the M2 anti-inflammatory phenotype.Our study also suggests that TREM2 might be a novel target for the intervention of obesity/diabetes-associated cognitive decline.展开更多
Ethylene response factor （ERF） proteins are important plant-specific transcription factors. Increasing evidence shows that ERF proteins regulate plant pathogen resistance, abiotic stress response and plant developme...Ethylene response factor （ERF） proteins are important plant-specific transcription factors. Increasing evidence shows that ERF proteins regulate plant pathogen resistance, abiotic stress response and plant development through interaction with different stress responsive pathways. Previously, we revealed that overexpression of TERF1 in tobacco activates a cluster gene expression through interacting with GCC box and dehydration responsive element （DRE）, resulting in enhanced sensitivity to abscisic acid （ABA） and tolerance to drought, and dark green leaves of mature plants, indicating that TERF1 participates in the integration of ethylene and osmotic responses. Here we further report that overexpression of TERF1 confers sugar response in tobacco. Analysis of the novel isolated tomato TERF1 promoter provides information indicating that there are many cis-acting elements, including sugar responsive elements （SURE） and W box, suggesting that TERF1 might be sugar inducible. This prediction is confirmed by results of reverse transcription-polymerase chain reaction amplification, indicating that transcripts of TERF1 are accumulated in tomato seedlings after application of glucose. Further investigation indicates that the expression of TERF1 in tobacco enhances sensitivity to glucose during seed germination, root and seedling development, showing a decrease of the fresh weight and root elongation under glucose treatment. Detailed investigations provide evidence that TERF1 interacts with the sugar responsive cis-acting element SURE and activates the expression of sugar response genes, establishing the transcriptional regulation of TERF1 in sugar response. Therefore, our results deepen our understanding of the glucose response mediated by the ERF protein TERF1 in tobacco.展开更多
Callus induction,which results in fate transition in plant cells,is considered as the first and key step for plant regeneration.This process can be stimulated in different tissues by a callus-inducing medium(CIM),whic...Callus induction,which results in fate transition in plant cells,is considered as the first and key step for plant regeneration.This process can be stimulated in different tissues by a callus-inducing medium(CIM),which contains a high concentration of phytohormone auxin.Although a few key regulators for callus induction have been identified,the multiple aspects of the regulatory mechanism driven by high levels of auxin still need further investigation.Here,we find that high auxin induces callus through a H3 K36 histone methylation-dependent mechanism,which requires the methyltransferase SET DOMAIN GROUP 8(SDG8).During callus induction,the increased auxin accumulates SDG8 expression through a TIR1/AFBs-based transcriptional regulation.SDG8 then deposits H3 K36 me3 modifications on the loci of callus-related genes,including a master regulator WOX5 and the cell proliferation-related genes,such as CYCB1.1.This epigenetic regulation in turn is required for the transcriptional activation of these genes during callus formation.These findings suggest that the massive transcriptional reprogramming for cell fate transition by auxin during callus formation requires epigenetic modifications including SDG8-mediated histone H3 K36 methylation.Our results provide insight into the coordination between auxin signaling and epigenetic regulation during fundamental processes in plant development.展开更多
Comparative gene identification-58(CGI-58),also known asα/βhydrolase domain containing 5,is the co-activator of adipose triglyceride lipase that hydrolyzes triglycerides stored in the cytosolic lipid droplets.Mutati...Comparative gene identification-58(CGI-58),also known asα/βhydrolase domain containing 5,is the co-activator of adipose triglyceride lipase that hydrolyzes triglycerides stored in the cytosolic lipid droplets.Mutations in CGI-58 gene cause Chanarin-Dorfman syndrome(CDS),an autosomal recessive neutral lipid storage disease with ichthyosis.The liver pathology of CDS manifests as steatosis and steatohepatitis,which currently has no effective treatments.Perilipin-3(Plin3)is a member of the Perilipin-ADRP-TIP47 protein family that is essential for lipid droplet biogenesis.The objective of this study was to test a hypothesis that deletion of a major lipid droplet protein alleviates fatty liver pathogenesis caused by CGI-58 deficiency in hepatocytes.Adult CGI-58-floxed mice were injected with adeno-associated vectors simultaneously expressing the Cre recombinase and microRNA against Plin3 under the control of a hepatocyte-specific promoter,followed by high-fat diet feeding for 6 weeks.Liver and blood samples were then collected from these animals for histological and biochemical analysis.Plin3 knockdown in hepatocytes prevented steatosis,steatohepatitis,and necroptosis caused by hepatocyte CGI-58 deficiency.Our work is the first to show that inhibiting Plin3 in hepatocytes is sufficient to mitigate hepatocyte CGI-58 deficiency-induced hepatic steatosis and steatohepatitis in mice.展开更多
The regulation ofβ-cell mass in the status of nondiabetic obesity remains not well understood.We aimed to investigate the role of circulating exosome-like vesicles(ELVs)isolated from humans with simple obesity in the...The regulation ofβ-cell mass in the status of nondiabetic obesity remains not well understood.We aimed to investigate the role of circulating exosome-like vesicles(ELVs)isolated from humans with simple obesity in the regulation of isletβ-cell mass.Between June 2017 and July 2019,81 subjects with simple obesity and 102 healthy volunteers with normal weight were recruited.ELVs were isolated by ultra-centrifugation.The proliferations ofβ-cells and islets were measured by 5-ethynl-2′-deoxyuridine(EdU).Protein components in ELVs were identified by Quantitative Proteomic Analysis and verified by Western blot and ELISA.The role of specific exosomal protein was analyzed by gain-of-function approach in ELVs released by 3T3-L1 preadipocytes.Circulating ELVs from subjects with simple obesity inhibitedβ-cell proliferation in vitro without affecting its apoptosis,secretion,and inflammation.The protein levels of Rictor and Omentin-1 were downregulated in circulating ELVs from subjects with simple obesity and associated with the obesity-linked pathologic conditions.The ELV-carried Omentin-1 and Omentin-1 protein per se were validated to increaseβ-cell proliferation and activate Akt signaling pathway.Moreover,Omentin-1 in ELVs was downregulated by insulin.The circulating ELVs may act as a negative regulator forβ-cell mass in nondiabetic obesity through inhibitingβ-cell proliferation.This effect was associated with downregulated Omentin-1 protein in ELVs.This newly identified ELV-carried protein could be a mediator linking insulin resistance to impairedβ-cell proliferation and a new potential target for increasingβ-cell mass in obesity and T2DM.展开更多
基金supported by the National Natural Science Foundation of China(31801335)Training Program for Excellent Young Innovators of Changsha(kq1802034)Department of Science and Technology in Hunan Province(2019RS2047).
文摘Plant architecture strongly influences rice grain yield.We report the cloning and characterization of the LTA1 gene,which simultaneously controls tiller angle and yield of rice.LTA1 encodes a chloroplastlocalized protein with a conserved YbaB DNA-binding domain,and is highly expressed in photosynthetic tissues including leaves and leaf sheaths.Disrupting the function of LTA1 leads to large tiller angle and yield reduction of rice.LTA1 affects the gravity response by mediating the distribution of endogenous auxin,thereby regulating the tiller angle.An lta1 mutant showed abnormal chloroplast development and decreased chlorophyll content and photosynthetic rate,in turn leading to reduction of rice yield.Our findings shed light on the genetic basis of tiller angle and provide a potential gene resource for the improvement of plant architecture and rice yield.
文摘Increasing evidence has revealed that abscisic acid （ABA） negatively modulates ethylene biosynthesis, although the underlying mechanism remains unclear. To identify the factors involved, we conducted a screen for ABA-insensitive mutants with altered ethylene production in Arabidopsis. A dominant allele of ABI4, abi4-152, which produces a putative protein with a 16-amino-acid truncation at the C-terminus of ABI4, reduces ethylene production. By contrast, two recessive knockout alleles of ABI4, abi4-102 and abi4-103, result in increased ethylene evolution, indicating that ABI4 negatively regulates ethylene produc- tion. Further analyses showed that expression of the ethylene biosynthesis genes ACS4, ACSS, and AC02 was significantly decreased in abi4-152 but increased in the knockout mutants, with partial dependence on ABA. Chromatin immunoprecipitation-quantitative PCR assays showed that ABI4 directly binds the pro- moters of these ethylene biosynthesis genes and that ABA enhances this interaction. A fusion protein containing the truncated ABI4-152 peptide accumulated to higher levels than its full-length counterpart in transgenic plants, suggesting that ABI4 is destabilized by its C terminus. Therefore, our results demon- strate that ABA negatively regulates ethylene production through ABI4-mediated transcriptional repression of the ethylene biosynthesis genes ACS4 and ACS8 in Arabidopsis.
基金This work was supported by the National Natural Science Foundation of China(No.81871222,81570763 and 81270947,to XX)the Fundamental Science and Advanced Technology Research of Chongqing(Major Project,No.CSTC2015jcyjB0146)the National Program on Key Basic Research Project(973 Program)of China(973 Program,No.2012CB517505,to XX).
文摘Type 2 diabetes mellitus(T2DM)and Alzheimer's disease(AD)share several common pathophysiological features.Rare variants of triggering receptor expressed on myeloid cells 2(TREM2)increase the risk of developing AD,suggesting the involvement of TREM2 and innate immunity in AD development.It is still unknown whether TREM2 is related to cognitive impairment in T2DM.Here,we investigated the effects of the hippocampal overexpression of TREM2 on cognitive in long-term high-fat diet(HFD)-fed mice.Male C57BL/6J mice were maintained on HFD for 50 weeks.TREM2 was overexpressed in the hippocampus 36 weeks after HFD feeding using adeno-associated virus vector(AAV)-mediated gene delivery.The results showed that the HFD feeding induced rapid and persistent weight gain,glucose intolerance and significant impairments in learning and memory.Compared with AAV-con,AAV-TREM2 significantly ameliorated cognitive impairment without altering body weight and glucose homeostasis in HFD mice.The overexpression of TREM2 upregulated the synaptic proteins spinophilin,PSD95 and synaptophysin,suggesting the improvement in synaptic transmission.Dendritic complexity and spine density in the CA1 region were rescued after TREM2 overexpression.Furthermore,TREM2 markedly increased the number of iba-1/Arg-1-positive microglia in the hippocampus,suppressed neuroinflammation and microglial activation.In sum,hippocampal TREM2 plays an important role in improving HFD-induced cognitive dysfunction and promoting microglial polarization towards the M2 anti-inflammatory phenotype.Our study also suggests that TREM2 might be a novel target for the intervention of obesity/diabetes-associated cognitive decline.
基金Supported by the National Natural Science Foundation of China (30525034)the State Key Basic Research and Development Plan of China(2006CB100102)
文摘Ethylene response factor （ERF） proteins are important plant-specific transcription factors. Increasing evidence shows that ERF proteins regulate plant pathogen resistance, abiotic stress response and plant development through interaction with different stress responsive pathways. Previously, we revealed that overexpression of TERF1 in tobacco activates a cluster gene expression through interacting with GCC box and dehydration responsive element （DRE）, resulting in enhanced sensitivity to abscisic acid （ABA） and tolerance to drought, and dark green leaves of mature plants, indicating that TERF1 participates in the integration of ethylene and osmotic responses. Here we further report that overexpression of TERF1 confers sugar response in tobacco. Analysis of the novel isolated tomato TERF1 promoter provides information indicating that there are many cis-acting elements, including sugar responsive elements （SURE） and W box, suggesting that TERF1 might be sugar inducible. This prediction is confirmed by results of reverse transcription-polymerase chain reaction amplification, indicating that transcripts of TERF1 are accumulated in tomato seedlings after application of glucose. Further investigation indicates that the expression of TERF1 in tobacco enhances sensitivity to glucose during seed germination, root and seedling development, showing a decrease of the fresh weight and root elongation under glucose treatment. Detailed investigations provide evidence that TERF1 interacts with the sugar responsive cis-acting element SURE and activates the expression of sugar response genes, establishing the transcriptional regulation of TERF1 in sugar response. Therefore, our results deepen our understanding of the glucose response mediated by the ERF protein TERF1 in tobacco.
基金the National Natural Science Foundation of China(Grant Nos 32130010,31422008,and 31870256)startup funds from FAFU to T.X.,and FAFU Youth Fund(Grant No.XJQ202016)to J.M.
文摘Callus induction,which results in fate transition in plant cells,is considered as the first and key step for plant regeneration.This process can be stimulated in different tissues by a callus-inducing medium(CIM),which contains a high concentration of phytohormone auxin.Although a few key regulators for callus induction have been identified,the multiple aspects of the regulatory mechanism driven by high levels of auxin still need further investigation.Here,we find that high auxin induces callus through a H3 K36 histone methylation-dependent mechanism,which requires the methyltransferase SET DOMAIN GROUP 8(SDG8).During callus induction,the increased auxin accumulates SDG8 expression through a TIR1/AFBs-based transcriptional regulation.SDG8 then deposits H3 K36 me3 modifications on the loci of callus-related genes,including a master regulator WOX5 and the cell proliferation-related genes,such as CYCB1.1.This epigenetic regulation in turn is required for the transcriptional activation of these genes during callus formation.These findings suggest that the massive transcriptional reprogramming for cell fate transition by auxin during callus formation requires epigenetic modifications including SDG8-mediated histone H3 K36 methylation.Our results provide insight into the coordination between auxin signaling and epigenetic regulation during fundamental processes in plant development.
基金supported by the National Natural Science Foundation of China(81873663 to Z.Z.).
文摘Comparative gene identification-58(CGI-58),also known asα/βhydrolase domain containing 5,is the co-activator of adipose triglyceride lipase that hydrolyzes triglycerides stored in the cytosolic lipid droplets.Mutations in CGI-58 gene cause Chanarin-Dorfman syndrome(CDS),an autosomal recessive neutral lipid storage disease with ichthyosis.The liver pathology of CDS manifests as steatosis and steatohepatitis,which currently has no effective treatments.Perilipin-3(Plin3)is a member of the Perilipin-ADRP-TIP47 protein family that is essential for lipid droplet biogenesis.The objective of this study was to test a hypothesis that deletion of a major lipid droplet protein alleviates fatty liver pathogenesis caused by CGI-58 deficiency in hepatocytes.Adult CGI-58-floxed mice were injected with adeno-associated vectors simultaneously expressing the Cre recombinase and microRNA against Plin3 under the control of a hepatocyte-specific promoter,followed by high-fat diet feeding for 6 weeks.Liver and blood samples were then collected from these animals for histological and biochemical analysis.Plin3 knockdown in hepatocytes prevented steatosis,steatohepatitis,and necroptosis caused by hepatocyte CGI-58 deficiency.Our work is the first to show that inhibiting Plin3 in hepatocytes is sufficient to mitigate hepatocyte CGI-58 deficiency-induced hepatic steatosis and steatohepatitis in mice.
基金This work was supported by the National Key R&D Program of China(No.2018YFA0800401)the National Natural Science Foundation of China(No.81200629,81570763,81770861 and 31571401)+2 种基金the Fundamental Science and Advanced Technology Research of Chongqing(Major Project,No.CSTC2015jcyjB0146)the Chongqing Science and Technology Foundation(No.cstc2018jcyjAX0232)the Science and Technology Research Program of Chongqing Municipal Education Commission(No.KJZD-K201800402).
文摘The regulation ofβ-cell mass in the status of nondiabetic obesity remains not well understood.We aimed to investigate the role of circulating exosome-like vesicles(ELVs)isolated from humans with simple obesity in the regulation of isletβ-cell mass.Between June 2017 and July 2019,81 subjects with simple obesity and 102 healthy volunteers with normal weight were recruited.ELVs were isolated by ultra-centrifugation.The proliferations ofβ-cells and islets were measured by 5-ethynl-2′-deoxyuridine(EdU).Protein components in ELVs were identified by Quantitative Proteomic Analysis and verified by Western blot and ELISA.The role of specific exosomal protein was analyzed by gain-of-function approach in ELVs released by 3T3-L1 preadipocytes.Circulating ELVs from subjects with simple obesity inhibitedβ-cell proliferation in vitro without affecting its apoptosis,secretion,and inflammation.The protein levels of Rictor and Omentin-1 were downregulated in circulating ELVs from subjects with simple obesity and associated with the obesity-linked pathologic conditions.The ELV-carried Omentin-1 and Omentin-1 protein per se were validated to increaseβ-cell proliferation and activate Akt signaling pathway.Moreover,Omentin-1 in ELVs was downregulated by insulin.The circulating ELVs may act as a negative regulator forβ-cell mass in nondiabetic obesity through inhibitingβ-cell proliferation.This effect was associated with downregulated Omentin-1 protein in ELVs.This newly identified ELV-carried protein could be a mediator linking insulin resistance to impairedβ-cell proliferation and a new potential target for increasingβ-cell mass in obesity and T2DM.
