Triacylglycerol(TAG)degradation plays an important role in seed oil accumulation,but how this catabolic process is transcriptionally regulated in developing seeds remains poorly understood.Here,we identify a MYB-like ...Triacylglycerol(TAG)degradation plays an important role in seed oil accumulation,but how this catabolic process is transcriptionally regulated in developing seeds remains poorly understood.Here,we identify a MYB-like helix-turn-helix(HTH)transcriptional regulator,PHR1-like 7(PHL7),that enhances TAG degradation and decreases seed oil accumulation in Arabidopsis thaliana.PHL7 knockout(KO)plants(phl7)exhibited an approximately 10%increase in seed oil content,whereas PHL7 overexpression(OE)decreased oil content by 8%-13%.Compared with wild-type plants,phl7 displayed reduced expression of TAG degradation genes,including SUGAR-DEPENDENT 1(SDP1),whereas OE lines exhibited elevated expression.Chromatin immunoprecipitation,electrophoretic mobility shift assays,and transactivation assays demonstrated that PHL7 binds the SDP1 promoter and activates its expression.We further found that PHL7 binds phosphatidic acid(PA),a key intermediate in TAG biosynthesis,and that PA suppresses PHL7 binding to the SDP1 promoter.The lysine residue at position 61(K61)is required for PA interaction,and introducing the PHL7 K61S mutation into phl7 failed to restore seed oil content to wild-type levels.Together,these findings indicate that PHL7 promotes SDP1 expression,whereas PA attenuates this activity,revealing a lipid-mediated mechanism that balances TAG degradation and seed oil accumulation.展开更多
Anthocyanin accumulation is acknowledged as a phenotypic indicator of phosphate(Pi)starvation.However,negative regulators of this process and their molecular mechanisms remain largely unexplored.In this study,we demon...Anthocyanin accumulation is acknowledged as a phenotypic indicator of phosphate(Pi)starvation.However,negative regulators of this process and their molecular mechanisms remain largely unexplored.In this study,we demonstrate that WRKY33 acts as a negative regulator of phosphorus-status-dependent anthocyanin biosynthesis.WRKY33 regulates the expression of the gene encoding dihydroflavonol 4-reductase(DFR),a rate-limiting enzyme in anthocyanin production,both directly and indirectly.WRKY33 binds directly to the DFR promoter to repress its expression and also interferes with the MBW complex through interacting with PAP1 to indirectly influence DFR transcriptional activation.Under�Pi conditions,PHR1 interacts with WRKY33,and the protein level of WRKY33 decreases;the repression of DFR expression by WRKY33 is thus attenuated,leading to anthocyanin accumulation in Arabidopsis.Further genetic and biochemical assays suggest that PHR1 is also involved in regulating factors that affect WRKY33 protein turnover.Taken together,ourfindings reveal that Pi starvation represses WRKY33,a repressor of anthocyanin biosynthesis,tofinely tune anthocyanin biosynthesis.This‘‘double-negative logic’’regulation of phosphorus-status-dependent anthocyanin biosynthesis is required for the mainte-nance of plant metabolic homeostasis during acclimation to Pi starvation.展开更多
PHR1(PHOSPHATE STARVATION RESPONSE1)plays key roles in the inorganic phosphate(Pi)starvation response and in Pi deficiency-induced anthocyanin biosynthesis in plants. However, the post-translational regulation of PHR1...PHR1(PHOSPHATE STARVATION RESPONSE1)plays key roles in the inorganic phosphate(Pi)starvation response and in Pi deficiency-induced anthocyanin biosynthesis in plants. However, the post-translational regulation of PHR1 is unclear,and the molecular basis of PHR1-mediated anthocyanin biosynthesis remains elusive. In this study, we determined that MdPHR1 was essential for Pi deficiency-induced anthocyanin accumulation in apple(Malus × domestica). MdPHR1 interacted with MdWRKY75, a positive regulator of anthocyanin biosynthesis, to enhance the MdWRKY75-activated transcription of MdMYB1,leading to anthocyanin accumulation. In addition,the E3 ubiquitin ligase SEVEN IN ABSENTIA1(MdSINA1) negatively regulated MdPHR1-promoted anthocyanin biosynthesis via the ubiquitination-mediated degradation of MdPHR1.Moreover, the protein kinase apple BRASSINOSTEROID INSENSITIVE2(MdBIN2) phosphorylated MdPHR1 and positively regulated MdPHR1-mediated anthocyanin accumulation by attenuating the MdSINA1-mediated ubiquitination degradation of MdPHR1. Taken together,these findings not only demonstrate the regulatory role of MdPHR1 in Pi starvation induced anthocyanin accumulation, but also provide an insight into the post-translational regulation of PHR1.展开更多
Phosphorus(P)is an essential nutrient for plant growth and reproduction.Plants preferentially absorb P as orthophosphate(Pi),an ion that displays low solubility and that is readily fixed in the soil,making P limita-ti...Phosphorus(P)is an essential nutrient for plant growth and reproduction.Plants preferentially absorb P as orthophosphate(Pi),an ion that displays low solubility and that is readily fixed in the soil,making P limita-tion a condition common to many soils and Pi fertilization an inefficient practice.To cope with Pi limitation,plants have evolved a series of developmental and physiological responses,collectively known as the Pi starvation rescue system(PSR),aimed to improve Pi acquisition and use efficiency(PUE)and protect from Pi-starvation-induced stress.Intensive research has been carried out during the last 20 years to un-ravel the mechanisms underlying the control of the PSR in plants.Here we review the results of this research effort that have led to the identification and characterization of several core Pi starvation signaling components,including sensors,transcription factors,microRNAs(miRNAs)and miRNA inhibitors,kinases,phosphatases,and components of the proteostasis machinery.We also refer to recent results revealing the existence of intricate signaling interplays between Pi and other nutrients and antagonists,N,Fe,Zn,and As,that have changed the initial single-nutrient-centric view to a more integrated view of nutrient homeostasis.Finally,we discuss advances toward improving PUE and future research priorities.展开更多
Arsenic is a metalloid toxic to plants,animals and human beings.Small ubiquitin-like modifier(SUMO)conjugation is involved in many biological processes in plants.However,the role of SUMOylation in regulating plant ars...Arsenic is a metalloid toxic to plants,animals and human beings.Small ubiquitin-like modifier(SUMO)conjugation is involved in many biological processes in plants.However,the role of SUMOylation in regulating plant arsenic response is still unclear.In this study,we found that dysfunction of SUMO E3 ligase SIZ1 improves arsenite resistance in Arabidopsis.Overexpression of the dominant-negative SUMO E2 variant resembled the arsenite-resistant phenotype of siz1 mutant,indicating that SUMOylation plays a negative role in plant arsenite detoxification.The siz1 mutant accumulated more glutathione(GSH)than the wild type under arsenite stress,and the arsenite-resistant phenotype of siz1 was depressed by inhibiting GSH biosynthesis.The transcript levels of the genes in the GSH biosynthetic pathway were increased in the siz1 mutant comparing with the wild type in response to arsenite treatment.Taken together,our findings revealed a novel function of SIZ1 in modulating plant arsenite response through regulating the GSH-dependent detoxification.展开更多
基金supported by the National Institute of General Medical Sciences of the National Institutes of Health under award numbers R01GM141374 and R35GM156366S.T.was supported in part by the Des Lee Collaborative Vision and a Postdoctoral Exchange Fellowship(no.PC2022027).
文摘Triacylglycerol(TAG)degradation plays an important role in seed oil accumulation,but how this catabolic process is transcriptionally regulated in developing seeds remains poorly understood.Here,we identify a MYB-like helix-turn-helix(HTH)transcriptional regulator,PHR1-like 7(PHL7),that enhances TAG degradation and decreases seed oil accumulation in Arabidopsis thaliana.PHL7 knockout(KO)plants(phl7)exhibited an approximately 10%increase in seed oil content,whereas PHL7 overexpression(OE)decreased oil content by 8%-13%.Compared with wild-type plants,phl7 displayed reduced expression of TAG degradation genes,including SUGAR-DEPENDENT 1(SDP1),whereas OE lines exhibited elevated expression.Chromatin immunoprecipitation,electrophoretic mobility shift assays,and transactivation assays demonstrated that PHL7 binds the SDP1 promoter and activates its expression.We further found that PHL7 binds phosphatidic acid(PA),a key intermediate in TAG biosynthesis,and that PA suppresses PHL7 binding to the SDP1 promoter.The lysine residue at position 61(K61)is required for PA interaction,and introducing the PHL7 K61S mutation into phl7 failed to restore seed oil content to wild-type levels.Together,these findings indicate that PHL7 promotes SDP1 expression,whereas PA attenuates this activity,revealing a lipid-mediated mechanism that balances TAG degradation and seed oil accumulation.
基金funded by the Zhejiang Provincial Natural Science Foundation of China under grant no.LR22C020003the National Key Research and Development Program of China (2022YFD2200603)+2 种基金the National Natural Science Foundation of China under grant nos.32000234 and 32172593the China Postdoctoral Science Foundation (2022M712831)funding from the State Key Laboratory for Managing Biotic and Chemical Threats to the Quality and Safety of Agro-products.
文摘Anthocyanin accumulation is acknowledged as a phenotypic indicator of phosphate(Pi)starvation.However,negative regulators of this process and their molecular mechanisms remain largely unexplored.In this study,we demonstrate that WRKY33 acts as a negative regulator of phosphorus-status-dependent anthocyanin biosynthesis.WRKY33 regulates the expression of the gene encoding dihydroflavonol 4-reductase(DFR),a rate-limiting enzyme in anthocyanin production,both directly and indirectly.WRKY33 binds directly to the DFR promoter to repress its expression and also interferes with the MBW complex through interacting with PAP1 to indirectly influence DFR transcriptional activation.Under�Pi conditions,PHR1 interacts with WRKY33,and the protein level of WRKY33 decreases;the repression of DFR expression by WRKY33 is thus attenuated,leading to anthocyanin accumulation in Arabidopsis.Further genetic and biochemical assays suggest that PHR1 is also involved in regulating factors that affect WRKY33 protein turnover.Taken together,ourfindings reveal that Pi starvation represses WRKY33,a repressor of anthocyanin biosynthesis,tofinely tune anthocyanin biosynthesis.This‘‘double-negative logic’’regulation of phosphorus-status-dependent anthocyanin biosynthesis is required for the mainte-nance of plant metabolic homeostasis during acclimation to Pi starvation.
基金financially supported by grants from the Natural Science Foundation of Shandong Province(ZR2022YQ24)the Development Plan of the Youth Innovation Team of the Higher Education Institutions in Shandong Province (2022KJ326)Wuhan Botanical Garden Scientific Research Support Project (E3559901)。
文摘PHR1(PHOSPHATE STARVATION RESPONSE1)plays key roles in the inorganic phosphate(Pi)starvation response and in Pi deficiency-induced anthocyanin biosynthesis in plants. However, the post-translational regulation of PHR1 is unclear,and the molecular basis of PHR1-mediated anthocyanin biosynthesis remains elusive. In this study, we determined that MdPHR1 was essential for Pi deficiency-induced anthocyanin accumulation in apple(Malus × domestica). MdPHR1 interacted with MdWRKY75, a positive regulator of anthocyanin biosynthesis, to enhance the MdWRKY75-activated transcription of MdMYB1,leading to anthocyanin accumulation. In addition,the E3 ubiquitin ligase SEVEN IN ABSENTIA1(MdSINA1) negatively regulated MdPHR1-promoted anthocyanin biosynthesis via the ubiquitination-mediated degradation of MdPHR1.Moreover, the protein kinase apple BRASSINOSTEROID INSENSITIVE2(MdBIN2) phosphorylated MdPHR1 and positively regulated MdPHR1-mediated anthocyanin accumulation by attenuating the MdSINA1-mediated ubiquitination degradation of MdPHR1. Taken together,these findings not only demonstrate the regulatory role of MdPHR1 in Pi starvation induced anthocyanin accumulation, but also provide an insight into the post-translational regulation of PHR1.
基金the Ministry of Science and Innovation,Spain(grant numbers BIO2017-89530-R and BIO2020-118750RB-100).
文摘Phosphorus(P)is an essential nutrient for plant growth and reproduction.Plants preferentially absorb P as orthophosphate(Pi),an ion that displays low solubility and that is readily fixed in the soil,making P limita-tion a condition common to many soils and Pi fertilization an inefficient practice.To cope with Pi limitation,plants have evolved a series of developmental and physiological responses,collectively known as the Pi starvation rescue system(PSR),aimed to improve Pi acquisition and use efficiency(PUE)and protect from Pi-starvation-induced stress.Intensive research has been carried out during the last 20 years to un-ravel the mechanisms underlying the control of the PSR in plants.Here we review the results of this research effort that have led to the identification and characterization of several core Pi starvation signaling components,including sensors,transcription factors,microRNAs(miRNAs)and miRNA inhibitors,kinases,phosphatases,and components of the proteostasis machinery.We also refer to recent results revealing the existence of intricate signaling interplays between Pi and other nutrients and antagonists,N,Fe,Zn,and As,that have changed the initial single-nutrient-centric view to a more integrated view of nutrient homeostasis.Finally,we discuss advances toward improving PUE and future research priorities.
基金supported by the National Natural Science Foundation of China(grant 32000206 to Z.W.)the Youth Innovation Promotion Association(2020273 to Z.W.)of the Chinese Academy of Sciences.
文摘Arsenic is a metalloid toxic to plants,animals and human beings.Small ubiquitin-like modifier(SUMO)conjugation is involved in many biological processes in plants.However,the role of SUMOylation in regulating plant arsenic response is still unclear.In this study,we found that dysfunction of SUMO E3 ligase SIZ1 improves arsenite resistance in Arabidopsis.Overexpression of the dominant-negative SUMO E2 variant resembled the arsenite-resistant phenotype of siz1 mutant,indicating that SUMOylation plays a negative role in plant arsenite detoxification.The siz1 mutant accumulated more glutathione(GSH)than the wild type under arsenite stress,and the arsenite-resistant phenotype of siz1 was depressed by inhibiting GSH biosynthesis.The transcript levels of the genes in the GSH biosynthetic pathway were increased in the siz1 mutant comparing with the wild type in response to arsenite treatment.Taken together,our findings revealed a novel function of SIZ1 in modulating plant arsenite response through regulating the GSH-dependent detoxification.
