Cell wall is the first physical barrier to aluminum(Al)toxicity.Modification of cell wall properties to change its binding capacity to Al is one of the major strategies for plant Al resistance;nevertheless,how it is r...Cell wall is the first physical barrier to aluminum(Al)toxicity.Modification of cell wall properties to change its binding capacity to Al is one of the major strategies for plant Al resistance;nevertheless,how it is regulated in rice remains largely unknown.In this study,we show that exogenous application of putrescines(Put)could significantly restore the Al resistance of art1,a rice mutant lacking the central regulator Al RESISTANCE TRANSCRIPTION FACTOR 1(ART1),and reduce its Al accumulation particularly in the cell wall of root tips.Based on RNA-sequencing,yeast-onehybrid and electrophoresis mobility shift assays,we identified an R2R3 MYB transcription factor OsMYB30 as the novel target in both ART1-dependent and Put-promoted Al resistance.Furthermore,transient dual-luciferase assay showed that ART1 directly inhibited the expression of OsMYB30,and in turn repressed Os4CL5-dependent 4-coumaric acid accumulation,hence reducing the Al-binding capacity of cell wall and enhancing Al resistance.Additionally,Put repressed OsMYB30 expression by eliminating Alinduced H2O2accumulation,while exogenous H2O2promoted OsMYB30 expression.We concluded that ART1 confers Put-promoted Al resistance via repression of OsMYB30-regulated modification of cell wall properties in rice.展开更多
Jasmonic acid(JA)is thought to be involved in plant responses to cadmium(Cd)stress,but the underlying molecular mechanisms are poorly understood.Here,we show that Cd treatment rapidly induces the expression of genes p...Jasmonic acid(JA)is thought to be involved in plant responses to cadmium(Cd)stress,but the underlying molecular mechanisms are poorly understood.Here,we show that Cd treatment rapidly induces the expression of genes promoting endogenous JA synthesis,and subsequently increases the JA concentration in Arabidopsis roots.Furthermore,exogenous methyl jasmonate(MeJA)alleviates Cd-generated chlorosis of new leaves by decreasing the Cd concentration in root cell sap and shoot,and decreasing the expression of the AtIRT1,AtHMA2 and AtHMA4 genes promoting Cd uptake and long-distance translocation,respectively.In contrast,mutation of a key JA synthesis gene,At AOS,greatly enhances the expression of AtIRT1,AtHMA2 and AtHMA4,increases Cd concentration in both roots and shoots,and confers increased sensitivity to Cd.Exogenous Me JA recovers the enhanced Cd-sensitivity of the ataos mutant,but not of atcoi1,a JA receptor mutant.In addition,exogenous Me JA reduces NO levels in Cd-stressed Arabidopsis root tips.Taken together,our results suggest that Cd-induced JA acts via the JA signaling pathway and its effects on NO levels to positively restrict Cd accumulation and alleviates Cd toxicity in Arabidopsis via suppression of the expression of genes promoting Cd uptake and long-distance translocation.展开更多
Modification of cell wall properties has been considered as one of the determinants that confer aluminum(Al)tolerance in plants,while how cell wall modifying processes are regulated remains elusive.Here,we present a W...Modification of cell wall properties has been considered as one of the determinants that confer aluminum(Al)tolerance in plants,while how cell wall modifying processes are regulated remains elusive.Here,we present a WRKY transcription factor WRKY47 involved in Al tolerance and root growth.Lack of WRKY47 significantly reduces,while overexpression of it increases Al tolerance.We show that lack of WRKY47 substantially affects subcellular Al distribution in the root,with Al content decreased in apoplast and increased in symplast,which is attributed to the reduced cell wall Al-binding capacity conferred by the decreased content of hemicellulose I in the wrky47-1 mutant.Based on microarray,real time-quantitative polymerase chain reaction and chromatin immunoprecipitation assays,we further show that WRKY47 directly regulates the expression of EXTENSIN-LIKE PROTEIN(ELP)and XYLOGLUCAN ENDOTRANSGLUCOSYLASE-HYDROLASES17(XTH17)responsible for cell wall modification.Increasing the expression of ELP and XTH17 rescued Al tolerance as well as root growth in wrky47-1 mutant.In summary,our results demonstrate that WRKY47 is required for root growth under both normal and Al stress conditions via direct regulation of cell wall modification genes,and that the balance of Al distribution between root apoplast and symplast conferred by WRKY47 is important for Al tolerance.展开更多
Iron(Fe)storage in plant seeds is not only necessary for seedling establishment following germination but is also a major source of dietary Fe for humans and other animals.Accumulation of Fe in seeds is known to be lo...Iron(Fe)storage in plant seeds is not only necessary for seedling establishment following germination but is also a major source of dietary Fe for humans and other animals.Accumulation of Fe in seeds is known to be low during early seed development.However,the underlying mechanism and biological significance remain elusive.Here,we show that reduced expression of Arabidopsis YABBY transcription factor INNER NO OUTER(INO)increases embryonic Fe accumulation,while transgenic overexpression of INO results in the opposite effect.INO is highly expressed during early seed development,and decreased INO expression increases the expression of NATURAL RESISTANCE-ASSOCIATED MACROPHAGE PROTEIN 1(NRAMP1),which encodes a transporter that contributes to seed Fe loading.The relatively high embryonic Fe accumulation conferred by decreased INO expression is rescued by the nramp1 loss-of-function mutation.We further demonstrated that INO represses NRAMP1 expression by binding to NRAMP1-specific promoter region.Interestingly,we found that excessive Fe loading into developing seeds of ino mutants results in greater oxidative damage,leading to increased cell death and seed abortion,a phenotype that can be rescued by the nramp1 mutation.Taken together,these results indicate that INO plays an important role in safeguarding reproduction by reducing Fe loading into developing seeds by repressing NRAMP1 expression.展开更多
Because Iron(Fe)is an essential element,Fe storage in plant seeds is necessary for seedling establishment following germination.However,the mechanisms controlling seed Fe storage during seed development remain largely...Because Iron(Fe)is an essential element,Fe storage in plant seeds is necessary for seedling establishment following germination.However,the mechanisms controlling seed Fe storage during seed development remain largely unknown.Here we reveal that an ERF95 transcription factor regulates Arabidopsis seed Fe accumulation.We show that expression of ERF95 increases during seed maturation,and that lack of ERF95 reduces seed Fe accumulation,consequently increasing sensitivity to Fe deficiency during seedling establishment.Conversely,overexpression of ERF95 has the opposite effects.We show that lack of ERF95 decreases abundance of FER1 messenger RNA in developing seed,which encodes Fe-sequestering ferritin.Accordingly,a fer1-1 loss-of-function mutation confers reduced seed Fe accumulation,and suppresses ERF95-promoted seed Fe accumulation.In addition,ERF95 binds to specific FER1 promoter GCC-boxes and transactivates FER1 expression.We show that ERF95 expression in maturing seed is dependent on EIN3,the master transcriptional regulator of ethylene signaling.While lack of EIN3 reduces seed Fe content,overexpression of ERF95 rescues Fe accumulation in the seed of ein3 loss-of-function mutant.Finally,we show that ethylene production increases during seed maturation.We conclude that ethylene promotes seed Fe accumulation during seed maturation via an EIN3-ERF95-FER1-dependent signaling pathway.展开更多
Plant hormone abscisic acid(ABA)plays an indispensable role in the control of leaf senescence,during which ABA signaling depends on its biosynthesis.Nevertheless,the role of ABA transport in leaf senescence remains un...Plant hormone abscisic acid(ABA)plays an indispensable role in the control of leaf senescence,during which ABA signaling depends on its biosynthesis.Nevertheless,the role of ABA transport in leaf senescence remains unknown.Here,we identified two novel RING-box protein-encoding genes UBIQUITIN LIGASE of SENESCENCE 1 and2(ULS1 and ULS2)involved in leaf senescence.Lack of ULS1 and ULS2 accelerates leaf senescence,which is specifically promoted by ABA treatment.Furthermore,the expression of senescence-related genes is significantly affected in mature leaves of uls1/uls2 double mutant(versus wild type(WT))in an ABA-dependent manner,and the ABA content is substantially increased.ULS1 and ULS2 are mainly expressed in the guard cells and aging leaves,and the expression is induced by ABA.Further RNA-seq and quantitative proteomics of ubiquitination reveal that ABA transporter ABCG40 is highly expressed in uls1/uls2 mutant versus WT,though it is not the direct target of ULS1/2.Finally,we show that the acceleration of leaf senescence,the increase of leaf ABA content,and the promotion of stomatal closure in uls1/usl2 mutant are suppressed by abcg40 loss-of-function mutation.These results indicate that ULS1 and ULS2 function in feedback inhibition of ABCG40-dependent ABA transport during ABA-induced leaf senescence and stomatal closure.展开更多
Unlike most crops,in which soil acidity severely limits productivity,tea(Camellia sinensis)actually prefers acid soils(pH 4.0–5.5).Specifically,tea is very tolerant of acidity-promoted aluminum(Al)toxicity,a major fa...Unlike most crops,in which soil acidity severely limits productivity,tea(Camellia sinensis)actually prefers acid soils(pH 4.0–5.5).Specifically,tea is very tolerant of acidity-promoted aluminum(Al)toxicity,a major factor that limits the yield of most other crops,and it even requires Al for optimum growth.Understanding tea Al tolerance and Al-stimulatory mechanisms could therefore be fundamental for the future development of crops adapted to acid soils.Here,we summarize the Al-tolerance mechanisms of tea plants,propose possible mechanistic explanations for the stimulation of tea growth by Al based on recent research,and put forward ideas for future crop breeding for acid soils.展开更多
基金supported by the National Natural Science Foundation of China(Grant No.31210103907)Guangdong Laboratory for Lingnan Modern Agriculture(Grant No.NT2021010)+1 种基金Research Program for Ecological Civilization and Innovation of Environmental Science and Technology in Zhejiang University,111 Project(Grant No.B14027)Grantin-Aid for Specially Promoted Research(JSPS KAKENHI Grant No.21H05034 to J.F.M.)。
文摘Cell wall is the first physical barrier to aluminum(Al)toxicity.Modification of cell wall properties to change its binding capacity to Al is one of the major strategies for plant Al resistance;nevertheless,how it is regulated in rice remains largely unknown.In this study,we show that exogenous application of putrescines(Put)could significantly restore the Al resistance of art1,a rice mutant lacking the central regulator Al RESISTANCE TRANSCRIPTION FACTOR 1(ART1),and reduce its Al accumulation particularly in the cell wall of root tips.Based on RNA-sequencing,yeast-onehybrid and electrophoresis mobility shift assays,we identified an R2R3 MYB transcription factor OsMYB30 as the novel target in both ART1-dependent and Put-promoted Al resistance.Furthermore,transient dual-luciferase assay showed that ART1 directly inhibited the expression of OsMYB30,and in turn repressed Os4CL5-dependent 4-coumaric acid accumulation,hence reducing the Al-binding capacity of cell wall and enhancing Al resistance.Additionally,Put repressed OsMYB30 expression by eliminating Alinduced H2O2accumulation,while exogenous H2O2promoted OsMYB30 expression.We concluded that ART1 confers Put-promoted Al resistance via repression of OsMYB30-regulated modification of cell wall properties in rice.
基金supported by National Key R&D Program of China(2016YFD0100704)111 project(B14027)fundamental research fund for central Universities.
文摘Jasmonic acid(JA)is thought to be involved in plant responses to cadmium(Cd)stress,but the underlying molecular mechanisms are poorly understood.Here,we show that Cd treatment rapidly induces the expression of genes promoting endogenous JA synthesis,and subsequently increases the JA concentration in Arabidopsis roots.Furthermore,exogenous methyl jasmonate(MeJA)alleviates Cd-generated chlorosis of new leaves by decreasing the Cd concentration in root cell sap and shoot,and decreasing the expression of the AtIRT1,AtHMA2 and AtHMA4 genes promoting Cd uptake and long-distance translocation,respectively.In contrast,mutation of a key JA synthesis gene,At AOS,greatly enhances the expression of AtIRT1,AtHMA2 and AtHMA4,increases Cd concentration in both roots and shoots,and confers increased sensitivity to Cd.Exogenous Me JA recovers the enhanced Cd-sensitivity of the ataos mutant,but not of atcoi1,a JA receptor mutant.In addition,exogenous Me JA reduces NO levels in Cd-stressed Arabidopsis root tips.Taken together,our results suggest that Cd-induced JA acts via the JA signaling pathway and its effects on NO levels to positively restrict Cd accumulation and alleviates Cd toxicity in Arabidopsis via suppression of the expression of genes promoting Cd uptake and long-distance translocation.
基金This work was supported by the Ministry of Science and Technology of China(Grant No.2015CB942903)the National Natural Science Foundation of China(Grant No.31500206,31730006)+2 种基金China Postdoctoral Science Foun-dation(Grant No.2017T100428)111 project(Grant No.B14027)the Fundamental Research Funds for the Central Universities。
文摘Modification of cell wall properties has been considered as one of the determinants that confer aluminum(Al)tolerance in plants,while how cell wall modifying processes are regulated remains elusive.Here,we present a WRKY transcription factor WRKY47 involved in Al tolerance and root growth.Lack of WRKY47 significantly reduces,while overexpression of it increases Al tolerance.We show that lack of WRKY47 substantially affects subcellular Al distribution in the root,with Al content decreased in apoplast and increased in symplast,which is attributed to the reduced cell wall Al-binding capacity conferred by the decreased content of hemicellulose I in the wrky47-1 mutant.Based on microarray,real time-quantitative polymerase chain reaction and chromatin immunoprecipitation assays,we further show that WRKY47 directly regulates the expression of EXTENSIN-LIKE PROTEIN(ELP)and XYLOGLUCAN ENDOTRANSGLUCOSYLASE-HYDROLASES17(XTH17)responsible for cell wall modification.Increasing the expression of ELP and XTH17 rescued Al tolerance as well as root growth in wrky47-1 mutant.In summary,our results demonstrate that WRKY47 is required for root growth under both normal and Al stress conditions via direct regulation of cell wall modification genes,and that the balance of Al distribution between root apoplast and symplast conferred by WRKY47 is important for Al tolerance.
基金This work was supported by the Ministry of Science and Technology of the People's Republic of China(grant no.2016YFD0100704)the Natural Science Foundation of Zhejiang Province(Q19C020001)+1 种基金the Ministry of Education and Bureau of Foreign Experts of China(grant no.B14027)the Fundamental Research Funds for the Central Universities.
文摘Iron(Fe)storage in plant seeds is not only necessary for seedling establishment following germination but is also a major source of dietary Fe for humans and other animals.Accumulation of Fe in seeds is known to be low during early seed development.However,the underlying mechanism and biological significance remain elusive.Here,we show that reduced expression of Arabidopsis YABBY transcription factor INNER NO OUTER(INO)increases embryonic Fe accumulation,while transgenic overexpression of INO results in the opposite effect.INO is highly expressed during early seed development,and decreased INO expression increases the expression of NATURAL RESISTANCE-ASSOCIATED MACROPHAGE PROTEIN 1(NRAMP1),which encodes a transporter that contributes to seed Fe loading.The relatively high embryonic Fe accumulation conferred by decreased INO expression is rescued by the nramp1 loss-of-function mutation.We further demonstrated that INO represses NRAMP1 expression by binding to NRAMP1-specific promoter region.Interestingly,we found that excessive Fe loading into developing seeds of ino mutants results in greater oxidative damage,leading to increased cell death and seed abortion,a phenotype that can be rescued by the nramp1 mutation.Taken together,these results indicate that INO plays an important role in safeguarding reproduction by reducing Fe loading into developing seeds by repressing NRAMP1 expression.
基金This work was supported by National Key Research and Development Program of China(2016YFD0100704)the Ministry of Education and Bureau of Foreign Experts of China(B14027)the Fundamental Research Funds for the Central Universities。
文摘Because Iron(Fe)is an essential element,Fe storage in plant seeds is necessary for seedling establishment following germination.However,the mechanisms controlling seed Fe storage during seed development remain largely unknown.Here we reveal that an ERF95 transcription factor regulates Arabidopsis seed Fe accumulation.We show that expression of ERF95 increases during seed maturation,and that lack of ERF95 reduces seed Fe accumulation,consequently increasing sensitivity to Fe deficiency during seedling establishment.Conversely,overexpression of ERF95 has the opposite effects.We show that lack of ERF95 decreases abundance of FER1 messenger RNA in developing seed,which encodes Fe-sequestering ferritin.Accordingly,a fer1-1 loss-of-function mutation confers reduced seed Fe accumulation,and suppresses ERF95-promoted seed Fe accumulation.In addition,ERF95 binds to specific FER1 promoter GCC-boxes and transactivates FER1 expression.We show that ERF95 expression in maturing seed is dependent on EIN3,the master transcriptional regulator of ethylene signaling.While lack of EIN3 reduces seed Fe content,overexpression of ERF95 rescues Fe accumulation in the seed of ein3 loss-of-function mutant.Finally,we show that ethylene production increases during seed maturation.We conclude that ethylene promotes seed Fe accumulation during seed maturation via an EIN3-ERF95-FER1-dependent signaling pathway.
基金supported by the Guangdong Laboratory of Lingnan Modern Agriculture Project(NT2021010)the Zhejiang Provincial Natural Science Foundation(LY21C020001)+2 种基金the Ministry of Education and Bureau of Foreign Experts of China(B14027)the ZJU Tang Scholar Foundationthe Fundamental Research Funds for the Central Universities。
文摘Plant hormone abscisic acid(ABA)plays an indispensable role in the control of leaf senescence,during which ABA signaling depends on its biosynthesis.Nevertheless,the role of ABA transport in leaf senescence remains unknown.Here,we identified two novel RING-box protein-encoding genes UBIQUITIN LIGASE of SENESCENCE 1 and2(ULS1 and ULS2)involved in leaf senescence.Lack of ULS1 and ULS2 accelerates leaf senescence,which is specifically promoted by ABA treatment.Furthermore,the expression of senescence-related genes is significantly affected in mature leaves of uls1/uls2 double mutant(versus wild type(WT))in an ABA-dependent manner,and the ABA content is substantially increased.ULS1 and ULS2 are mainly expressed in the guard cells and aging leaves,and the expression is induced by ABA.Further RNA-seq and quantitative proteomics of ubiquitination reveal that ABA transporter ABCG40 is highly expressed in uls1/uls2 mutant versus WT,though it is not the direct target of ULS1/2.Finally,we show that the acceleration of leaf senescence,the increase of leaf ABA content,and the promotion of stomatal closure in uls1/usl2 mutant are suppressed by abcg40 loss-of-function mutation.These results indicate that ULS1 and ULS2 function in feedback inhibition of ABCG40-dependent ABA transport during ABA-induced leaf senescence and stomatal closure.
基金supported by the Natural Science Foundation of China(grants 31730006 and 31572199)the 111 Project(B14027)the Fundamental Research Fund for the Central Universities.
文摘Unlike most crops,in which soil acidity severely limits productivity,tea(Camellia sinensis)actually prefers acid soils(pH 4.0–5.5).Specifically,tea is very tolerant of acidity-promoted aluminum(Al)toxicity,a major factor that limits the yield of most other crops,and it even requires Al for optimum growth.Understanding tea Al tolerance and Al-stimulatory mechanisms could therefore be fundamental for the future development of crops adapted to acid soils.Here,we summarize the Al-tolerance mechanisms of tea plants,propose possible mechanistic explanations for the stimulation of tea growth by Al based on recent research,and put forward ideas for future crop breeding for acid soils.