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A Light-Independent Allele of Phytochrome B Faithfully Recapitulates Photomorphogenic Transcriptional Networks

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molecular Plant 2009年第1期2卷 166-182页

作者： Wei Hu Yi-Shin Su J. Clark Lagarias department of molecular and cellular biology College of Biological Sciences University of California Davis CA 95616 USA present address: Carnegie Institution of Washington -Department of Plant Biology Stanford CA 94305 USA

Dominant gain-of-function alleles of Arabidopsis phytochrome B were recently shown to confer lightindependent, constitutive photomorphogenic （cop） phenotypes to transgenic plants （Su and Lagarias, 2007）. In the present study, comparative transcription profiling experiments were performed to assess whether the pattern of gene expression regulated by these alleles accurately reflects the process of photomorphogenesis in wild-type Arabidopsis. Whole- genome transcription profiles of dark-grown phyAphyB seedlings expressing the Y^276H mutant of phyB （YHB） revealed that YHB reprograms about 13% of the Arabidopsis transcriptome in a light-independent manner. The YHB-regulated transcriptome proved qualitatively similar to but quantitatively greater than those of wild-type seedlings grown under 15 or 50 μmol m^-2 m^-1 continuous red light （Rc）. Among the 2977 genes statistically significant two-fold （SSTF） regulated by YHB in the absence of light include those encoding components of the photosynthetic apparatus, tetrapyrrole/pigment biosynthetic pathways, and early light-responsive signaling factors. Approximately 80% of genes SSTF regulated by Rc were also YHB-regulated. Expression of a notable subset of 346 YHB-regulated genes proved to be strongly attenuated by Rc, indicating compensating regulation by phyC-E and/or other Rc-dependent processes. Since the majority of these 346 genes are regulated by the circadian clock, these results suggest that phyA- and phyB-independent light signaling pathway（s） strongly influence clock output. Together with the unique plastid morphology of dark-grown YHB seedlings, these analyses indicate that the YHB mutant induces constitutive photomorphogenesis via faithful reconstruction of phyB signaling pathways in a light-independent fashion.

关键词： light signaling signal transduction transcriptome analysis photomorphogenesis Arabidopsis phytochrome.

Emerging Perspectives on the Mechanisms, Regulation, and Distribution of Light Color Acclimation in Cyanobacteria

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molecular Plant 2012年第1期5卷 1-13页

作者： Andrian Gutu David M. Kehoe department of biology 1001 East Third Street indiana University Bloomington iN 47405 USA present address： HoWard Hughes Medical Institute/department Of molecular and cellular biology FAS Center for Systems Biology Harvard UniversityCambridge MA 02138 USA

Chromatic acclimation （CA） provides many cyanobacteria with the ability to tailor the properties of their light-harvesting antennae to the spectral distribution of ambient light. CA was originally discovered as a result of its dramatic cellular phenotype in red and green light. However, discoveries over the past decade have revealed that many pairs of light colors, ranging from blue to infrared, can trigger CA responses. The capacity to undergo CA is widespread geographically, occurs in most habitats around the world, and is found within all major cyanobacterial groups. In addition, many other cellular activities have been found to be under CA control, resulting in distinct physiological and morphological states for cells under different light-color conditions. Several types of CA appear to be the result of convergent evolution, where different strategies are used to achieve the final goal of optimizing light-harvesting antenna composition to maximize photon capture. The regulation of CA has been found to occur primarily at the level of RNA abundance. The CA-regulatory pathways uncovered thus far are two-component systems that use phytochrome-class photoreceptors with sensor-kinase domains to control response regulators that function as transcription factors. However, there is also at least one CA- regulatory pathway that operates at the post-transcriptional level. It is becoming increasingly clear that large numbers of cyanobacterial species have the capacity to acclimate to a wide variety of light colors through the use of a range of different CA processes.

关键词： Chromatic adaptation phycobilisome cyanobacteria light regulation gene regulation signal transduction light harvesting phenotypic plasticity.

The WAK-like protein RFO1 acts as a sensor of the pectin methylation status in Arabidopsis cell walls to modulate root growth and defense

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molecular Plant 2023年第5期16卷 865-881页

作者： Apolonio I.Huerta Gloria Sancho-Andre´s Juan Carlos Montesinos Javier Silva-Navas Sole`ne Bassard Corinne Pau-Roblot Christopher Kesten Rudolf Schlechter Susanne Dora Temurkhan Ayupov Je´rome Pelloux^ Julia Santiago Clara Sa´nchez-Rodrı´guez ETH Zurich Institute of Molecular Plant Biology(D-BIOL)ZurichSwitzerland University of Lausanne Department of Plant Molecular BiologyLausanneSwitzerland UMRT INRAE 1158 BioEcoAgro–BIOPI Biologie des Plantes et Innovation Universite´de Picardie33 Rue St Leu80039 AmiensFrance present address:Lonza AG VispVisSwitzerland present address:Institute of Microbiology Freie Universitat BerlinBerlinGermany present address:Institute of molecular and Clinical Ophthalmology-Basel BaselSwitzerland present address:Centro de Biotecnologı´a y Geno´mica de Plantas Universidad Polite´cnica de Madrid(UPM)–Instituto Nacional de Investigacio´n y Tecnologı´a Agraria y Alimentaria(INIA/CSIC)Campus de Montegancedo UPM28223 Pozuelo de Alarco´nSpain

Most organisms adjust their development according to the environmental conditions.For the majority,this implies the sensing of alterations to cell walls caused by different cues.Despite the relevance of this process,few molecular players involved in cell wall sensing are known and characterized.Here,we show that the wall-associated kinase-like protein RESISTANCE TO FUSARIUM OXYSPORUM 1(RFO1)is required for plant growth and early defense against Fusarium oxysporum and functions by sensing changes in the pectin methylation levels in the cell wall.The RFO1 dwell time at the plasma membrane is affected by the pectin methylation status at the cell wall,regulating MITOGEN-ACTIVATED PROTEIN KINASE and gene expression.We show that the extracellular domain of RFO1 binds de-methylated pectin in vitro,whose distribution in the cell wall is altered during F.oxysporum infection.Further analyses also indicate that RFO1 is required for the BR-dependent plant growth alteration in response to inhibition of pectin de-methyl-esterase activity at the cell wall.Collectively,our work demonstrates that RFO1 is a sensor of the pectin methylation status that plays a unique dual role in plant growth and defense against vascular pathogens.

关键词： alterations walls pectin

Modular Synthesis of Multi-substituted Cyclobutanones Enabled by Oxyallyl Cations

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Chinese Journal of Chemistry 2024年第5期42卷 459-463页

作者： Meng Wang Zhonggui Wang Ping Lu Research Center for molecular Recognition and Synthesis Department of ChemistryFudan University220 Handan LuShanghai200433 China present address: department of Cancer biology Dana-Farber Cancer Institute department of Biological Chemistry and molecular Pharmacology Harvard Medical SchoolBostonMA 02115USA

Stereoselective synthesis of multi-substituted cyclobutanes with different substituents is still a daunting challenge in organic synthesis.We report here a practical and facile approach to synthesizing all-trans 2,3,4-trisubstituted cyclobutanones from readily available dichlorocyclobutanones.The substitution reaction proceeds smoothly via oxyallyl cation intermediates under mild basic conditions.Further transformation to the synthesis of 1,2,3,4-tetrasubstituted cyclobutanes was also explored.

关键词： Diastereoselectivity Modular synthesis Nucleophilic substitution Organohalides Oxyallyl cation Precision functionalization Strained molecules 1,2,3,4-Tetrasubstituted cyclobutanes

Immunophilin-like FKBP42/TWISTED DWARF1 Interacts with the Receptor Kinase BRI1 to Regulate Brassinosteroid Signaling in Arabidopsis

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molecular Plant 2016年第4期9卷 593-600页

作者： Juthamas Chaiwanon Veder J. Garcia Heather Cartwright Ying Sun Zhi-Yong Wang department of Plant biology Carnegie Institution for Science Stanford CA 94305 USA department of Botany Center of Excellence in Environment and Plant Physiology Faculty of Science Chulalongkorn University Bangkok 10330 Thailand present address: Institute of molecular Cell biology Hebei Key Laboratory of Molecular and Cellular Biology Hebei Normal University Shijiazhuang 050024 China

Mutation of the immunophilin-like FK506-binding protein TWlSTED DWARF1 （FKBP42/TWD1） causes dwarf and twisted-organ phenotypes in Arabidopsis. However, the function of FKBP42 is not fully understood at the molecular level. Using genetic, physiological, and immunological experiments, we show here that FKBP42/TWD1 is necessary for brassinosteroid （BR） signal transduction. The twdl mutant showed reduced BR sensitivity in growth responses and activation of the BZR1 transcription factor. However, twdl showed normal responses to an inhibitor of BIN2/GSK3, suggesting that twdl has a defect upstream of BIN2 in the BR signaling pathway. In vitro and in vivo assays showed that TWD1 interacts physically with the kinase domains of the BR receptor kinases BRI1 and BAK1. TWD1 is not required for normal localization of BRI1-GFP to the plasma membrane or for activation of the flagellin receptor kinase FLS2. Our results suggest that FKBP42/TWD1 plays a specific role in the activation of BRI1 receptor kinase.

关键词： brassinosteroid signaling BRI1 FKBP42

Functional Analysis of Semi-conserved Transit Peptide Motifs and Mechanistic Implications in Precursor Targeting and Recognition

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molecular Plant 2016年第9期9卷 1286-1301页

作者： Kristen Holbrook Chitra Subramanian Prakitchai Chotewutmontri L. Evan Reddick Sarah Wright Huixia Zhang Lily Moncrief Barry D. Bruce department of Biochemistry Cellular and Molecular Biology Graduate Program in Plant Physiology and Genetics Graduate School of Genome Science and Technology department of Botany department of BotanyUniversity of Tennessee Knoxville TN 37996 USA present address: department of Infectious Disease St. Jude Children's Research Hospital Memphis TN 38105 USA present address: Institute of molecular biology University of Oregon Eugene OR 97403 USA present address: department of Microbiology University of Texas Southwestern Medical Center 5323 Harry Hines Boulevard Dallas TX 75390 USA present address: Albert R. Mann Library Cornell University Ithaca NY 14850 USA present address: U.S. Food and Drug Administration 10903 New Hampshire Avenue Silver Spring MD 20993 USA

Over 95% of plastid proteins are nuclear-encoded as their precursors containing an N-terminal extension known as the transit peptide （TP）. Although highly variable, TPs direct the precursors through a conserved, posttranslational mechanism involving translocons in the outer （TOC） and inner envelope （TOC）. The organelle import specificity is mediated by one or more components of the Toc complex. However, the high TP diversity creates a paradox on how the sequences can be specifically recognized. An emerging model of TP design is that they contain multiple loosely conserved motifs that are recognized at different steps in the targeting and transport process. Bioinformatics has demonstrated that many TPs contain semiconserved physicochemical motifs, termed FGLK. In order to characterize FGLK motifs in TP recognition and import, we have analyzed two well-studied TPs from the precursor of RuBisCO small subunit （SStp） and ferredoxin （Fdtp）. Both SStp and Fdtp contain two FGLK motifs. Analysis of large set mutations （-85） in these two motifs using in vitro, in organello, and in vivo approaches support a model in which the FGLK domains mediate interaction with TOC34 and possibly other TOC components. In vivo import analysis suggests that multiple FGLK motifs are functionally redundant. Furthermore, we discuss how FGLK motifs are required for efficient precursor protein import and how these elements may permit a convergent function of this highly variable class of targeting sequences.

关键词： chloroplast biology protein translocation Toc34 transit peptide cell biology

Differential alterations of positive and negative regulators of beta catenin enhance endogenous expression and activity of beta catenin in A549 non small cell lung cancer(NSCLC)cells

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Genes & Diseases 2016年第4期3卷 282-288页

作者： Supratim Ghatak Sanghamitra Raha Crystallography and molecular biology Division Saha Institute of Nuclear Physics1/AF BidhannagarKolkata 700064India department of Biotechnology and ISERC Visva Bharati UniversitySantiniketan731235India present address:Centre for cellular and molecular biology Uppal RoadHyderabad 500007India

Beta catenin has been well documented in previous studies to be involved in non small cell lung cancer(NSCLC).Beta catenin abundance and transcriptional activity are significantly regulated by several factors.Though it is well known that Akt and Gsk3 beta are respective positive and negative regulators of beta catenin,however,no single study has so far documented how the expression and activity of both positive as well as negative regulators play favorable role on beta catenin expression and activity in NSCLC.In this study,we compared expression and activity of beta catenin and its regulators in normal lung cell WI38 and NSCLC cell A549 by western blot,qRT-PCR and luciferase assay.We observed that beta catenin positive regulators(Akt and Hsp90)and negative regulators(Gsk3 beta and microRNA-214)have differential expression and/or activity in NSCLC cell A549.However the differentially altered statuses of both the positive and negative regulators rendered cumulative positive effect on beta catenin expression and activity in A549.Our study thus suggests that chemotherapeutic modulations of regulating factors are crucial when abrogation and/or inhibition of key oncogenic proteins are necessary for cancer chemotherapy.

关键词： A549 Beta catenin Gsk3 beta miR-214 Non small cell lung cancer

MicroRNAs as diagnostic markers and therapeutic targets for traumatic brain injury

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Neural Regeneration Research 2017年第11期12卷 1749-1761页

作者： Bridget Martinez Philip V.Peplow department of molecular and cellular biology University of California department of Anatomy University of Otago

Traumatic brain injury （TBI） is characterized by primary damage to the brain from the external mechanical force and by subsequent secondary injury due to various molecular and pathophysiological responses that eventually lead to neuronal cell death. Secondary brain injury events may occur minutes, hours, or even days after the trauma, and provide valuable therapeutic targets to prevent further neuronal degeneration. At the present time, there is no effective treatment for TBI due, in part, to the widespread impact of numerous complex secondary biochemical and pathophysiological events occurring at different time points following the initial injury. MicroRNAs control a range of physiological and pathological functions such as develop- ment, differentiation, apoptosis and metabolism, and may serve as potential targets for progress assessment and intervention against TBI to mitigate secondary damage to the brain. This has implications regarding improving the diagnostic accuracy of brain impairment and long-term outcomes as well as potential novel treatments. Recent human studies have identified specific microRNAs in serum/plasma （miR-425-p, -21, -93, -191 and -499） and cerebro-spinal fluid （CSF）（miR-328, -362-3p, -451, -486a） as possible indicators of the diagnosis, severity, and prognosis of TBI. Experimental animal studies have examined specific microRNAs as biomarkers and therapeutic targets for moderate and mild TBI （e.g., miR-21, miR-23b）. MicroRNA profil- ing was altered by voluntary exercise. Differences in basal microRNA expression in the brain of adult and aged animals and alterations in response to TBI （e.g., miR-21） have also been reported. Further large-scale studies with TBI patients are needed to provide more information on the changes in microRNA profiles in different age groups （children, adults, and elderly）.

关键词： traumatic brain injury microRNAs diagnostic markers therapeutic targets： humans animal models

Inhibition of tumor suppressor p73 by nerve growth factor receptor via chaperone-mediated autophagy

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Journal of molecular Cell biology 2020年第9期12卷 700-712页

作者： Daniel Nguyen Kun Yang Lucia Chiao Yun Deng Xiang Zhou Zhen Zhang Shelya X.Zeng Hua Lu department of Biochemistry and molecular biology Tulane Cancer CenterTulane University School of MedicineNew OrleansLA 70112USA department of Radiation Oncology Shanghai Cancer CenterDepartment of OncologyShanghai Medical SchoolFudan UniversityShanghai 200032China present address:Verna and Marrs McLean department of Biochemistry and molecular biology Baylor College of MedicineHoustonTX 77030USA present address:department of Radiation Oncology Shanghai Cancer CenterFudan UniversityShanghai 200032China present address:Institute of Biomedical Sciences Shanghai Cancer CenterFudan UniversityShanghai 200032China

The tumor suppressr p73 is a homolog of p53 and is capable of inducing cell cycle arrest and apoptosis.Here,we identify nerve growth factor receptor(NGFR,p75NTR,or CD271)as a novel negative p73 regulator.p73 activates NGFR transcription,which,in turn,promotes p73 degradation in a negative feedback loop.NGFR directly binds to p73 central DNA-binding domain and suppresses p73 transcriptional activity as well as p73-mediated apoptosis in cancer cells.Surprisingly,we uncover a previously unknown mechanism of NGFR-facilitated p73 degradation through the chaperone-mediated autophagy(CMA)pathway.Collectively,our studies demonstrate a new oncogenic function for NGFR in inactivating p73 activity by promoting its degradation through the CMA.

关键词： p73 NGFR chaperone-mediated autophagy Lamp2a HSPA8