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Arogenate Dehydratase Isoforms Differentially Regulate Anthocyanin Biosynthesis in Arabidopsis thaliana

Molecular Plant 2016年第12期9卷 1609-1619页

作者： Qingbo Chen Cong Man Danning Li Huijuan Tan Ye Xie Jirong Huang National Key Laboratory of Plant Molecular Genetics CAS Center for Excellence in Molecular Plant Sciences Shanghai Institute of Plant Physiology and Ecology Chinese Academy of Sciences 300 Fenglin Road Shanghai 200032 China These authors contributed equally to this article

Anthocyanins, a group of L-phenylalanine （Phe）-derived flavonoids, have been demonstrated to play impor- tant roles in plant stress resistance and interactions between plants and insects. Although the anthocyanin biosynthetic pathway and its regulatory mechanisms have been extensively studied, it remains unclear whether the level of Phe supply affects anthocyanin biosynthesis. Here, we investigated the roles of arogenate dehydratases （ADTs）, the key enzymes that catalyze the conversion of arogenate into Phe, in sucrose-induced anthocyanin biosynthesis in Arabidopsis. Genetic analysis showed that all six ADT isoforms function redundantly in anthocyanin biosynthesis but have differential contributions. ADT2 contributes the most to anthocyanin accumulation, followed by ADT1 and ADT3, and ADT4-ADT6. We found that anthocyanin content is positively correlated with the levels of Phe and sucrose-induced ADT transcripts in seedlings. Consistently, addition of Phe to the medium could dramatically increase anthocyanin content in the wild-type plants and rescue the phenotype of the adtl adt3 double mutant regarding the anthocyanin accumulation. Moreover, transgenic plants overexpressing ADT4, which appears to be less sensitive to Phe than overexpression ofADT2, hyperaccumulate Phe and produce elevated level of antho- cyanins. Taken together, our results suggest that the level of Phe is an important regulatory factor for sus- taining anthocyanin biosynthesis.

关键词： phenylalanine metabolic flux ADT anthocyanin Arabidopsis

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Contribution of phenylpropanoid metabolism to plant development and plant–environment interactions

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Journal of Integrative Plant Biology 2021年第1期63卷 180-209页

作者： Nai-Qian Dong Hong-Xuan Lin National Key Laboratory of Plant Molecular Genetics CAS Centre for Excellence in Molecular Plant Sciences and Collaborative Innovation Center of Genetics and DevelopmentShanghai Institute of Plant Physiology and Ecologythe Chinese Academy of SciencesShanghai 200032China University of the Chinese Academy of Sciences Beijing 100049China School of Life Science and Technology ShanghaiTech UniversityShanghai 201210China

Phenylpropanoid metabolism is one of the most important metabolisms in plants, yielding more than 8,000 metabolites contributing to plant development and plant-environment interplay.Phenylpropanoid metabolism materialized during the evolution of early freshwater algae that were initiating terrestrialization and land plants have evolved multiple branches of this pathway, which give rise to metabolites including lignin, flavonoids, lignans, phenylpropanoid esters, hydroxycinnamic acid amides, and sporopollenin.Recent studies have revealed that many factors participate in the regulation of phenylpropanoid metabolism, and modulate phenylpropanoid homeostasis when plants undergo successive developmental processes and are subjected to stressful environments. In this review, we summarize recent progress on elucidating the contribution of phenylpropanoid metabolism to the coordination of plant development and plant–environment interaction, and metabolic flux redirection among diverse metabolic routes. In addition, our review focuses on the regulation of phenylpropanoid metabolism at the transcriptional, post-transcriptional, post-translational,and epigenetic levels, and in response to phytohormones and biotic and abiotic stresses.

关键词： flavonoids lignin metabolic flux phenylpropanoid secondary metabolites

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metabolic reprogramming in tumors:Contributions of the tumor microenvironment

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Genes & Diseases 2020年第2期7卷 185-198页

作者： Andrew N.Lane Richard M.Higashi Teresa W-M.Fan Center for Environmental and Systems Biochemistry Markey Cancer CenterDepartment of Toxicology and Cancer BiologyUniversity of KentuckyUSA

The genetic alterations associated with cell transformation are in large measure expressed in the metabolic phenotype as cancer cells proliferate and change their local environment,and prepare for metastasis.Qualitatively,the fundamental biochemistry of cancer cells is generally the same as in the untransformed cells,but the cancer cells produce a local environment,the TME,that is hostile to the stromal cells,and compete for nutrients.In order to proliferate,cells need sufficient nutrients,either those that cannot be made by the cells themselves,or must be made from simpler precursors.However,in solid tumors,the nutrient supply is often limiting given the potential for rapid proliferation,and the poor quality of the vasculature.Thus,cancer cells may employ a variety of strategies to obtain nutrients for survival,growth and metastasis.Although much has been learned using established cell lines in standard culture conditions,it is becoming clear from in vivo metabolic studies that this can also be misleading,and which nutrients are used for energy production versus building blocks for synthesis of macromolecules can vary greatly from tumor to tumor,and even within the same tumor.Here we review the operation of metabolic networks,and how recent understanding of nutrient supply in the TME and utilization are being revealed using stable isotope tracers in vivo as well as in vitro.

关键词： Cancer metabolism Nutrient supply Stable isotope resolved metabolomics Tumor microenvironment metabolic flux

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Metabolomics profiling of metformin-mediated metabolic reprogramming bypassing AMPKα

Metabolomics profiling of metformin-mediated metabolic repro...

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第三届中国生物物理学会代谢生物学分会学术研讨会

作者： Min Yan Huan Qi Hai-long Piao CAS Key Laboratory of Separation Science for Analytical Chemistry Scientific Research Center for Translational MedicineDalian Institute of Chemical PhysicsChinese Academy of Sciences 中国科学院大连化学物理研究所

Metformin is a first-line drug for treating type 2 diabetes and has gained considerable interest as a potential anticancer agent.Increasing evidence suggests that metformin antagonizes diabetes and tumors through disrupting metabolic homeostasis and altering energy state.However,whether AMP activated protein kinase(AMPK) contributes to such effects of metformin remains controversial.Here,we performed integrative metabolomics analyses to systematically examine the effects of metformin on metabolic pathways in Prkaal wild type(WT) and knock-out(KO) mouse embryonic fibroblast(MEF) cells based on gas chromatography-mass spectrometry and capillary electrophoresis-mass spectrometry(CE-MS).Metformin treatment induced metabolic reprogramming and reduced the energy state of both Prkaa1 WT and KO MEF cells,as evidenced by suppressed tricarboxylic acid(TCA) cycle,elevated lactate production as well as decreased NAD/NADH ratio.Additionally,metabolic flux analysis also showed that metformin Ampka-independently increased metabolic flux from glucose to lactate and decreased metabolic flux from acetyl-CoA to TCA cycle as well as from pyruvate to malate.Moreover,metformin Ampka-dependently upregulated P-Acc but Ampkα-independently inhibited the levels of P-mTOR,P-S6,Lc3,Atgl and P-Erk in MEF cells.Similarly,we demonstrated that a commonly used AMPK agonist 5-Aminoimidazole-4-carboxamide ribonucleotide(AICAR) and fetal bovine serum(FBS)starvation,as a common model for energy stress,both led to Ampkα-independent metabolism alterations in MEF cells.Furthermore,these effects of metformin were also confirmed in human hepatocellular carcinoma(HCC) cells as well as in MCF10 A shControl and shPRKAAl cells.Importantly,we found that metformin could obviously inhibit colony conformation of HCC cells in an Ampkα-independent manner.Our data highlight a comprehensive view of metabolomics reprogramming mediated by metformin as well as AICAR.These observations suggest that metformin could affect cellular metabolism largely bypassing Ampkα,and ma

关键词： Metformin Ampk Metabolomics metabolic flux Independence

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