Transcriptional profiling of sunflower plants growing under low temperatures reveals an extensive down-regulation of gene expression associated with chilling sensitivity

We dissected the promoter of the developmentally induced and cyclic AMP-repressed discoidin I gamma gene and identified a sequence element essential for developmental induction. Transfer of the element to an inactive heterologous promoter demonstrated that this sequence is sufficient to confer expression in axenically growing cells and to induce gene activity in development after growth on bacteria. A 16-base-pair sequence within this element was shown to be sufficient for induction in the discoidin promoter context and was used to reactivate different truncated promoter constructs. This led to the localization of an element necessary for down regulation of gene expression by extracellular cyclic AMP.

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Regulation of the Discoidin I gamma gene in Dictyostelium discoideum: identification of individual promoter elements mediating induction of transcription and repression by cyclic AMP.

Molecular and Cellular Biology ◽

10.1128/mcb.10.8.4080 ◽

1990 ◽

Vol 10 (8) ◽

pp. 4080-4088 ◽

Cited By ~ 43

Author(s):

F Vauti ◽

P Morandini ◽

J Blusch ◽

A Sachse ◽

W Nellen

Keyword(s):

Gene Expression ◽

Cyclic Amp ◽

Dictyostelium Discoideum ◽

Base Pair ◽

Regulation Of Gene Expression ◽

Promoter Elements ◽

Down Regulation ◽

Heterologous Promoter ◽

Sequence Element ◽

Pair Sequence

We dissected the promoter of the developmentally induced and cyclic AMP-repressed discoidin I gamma gene and identified a sequence element essential for developmental induction. Transfer of the element to an inactive heterologous promoter demonstrated that this sequence is sufficient to confer expression in axenically growing cells and to induce gene activity in development after growth on bacteria. A 16-base-pair sequence within this element was shown to be sufficient for induction in the discoidin promoter context and was used to reactivate different truncated promoter constructs. This led to the localization of an element necessary for down regulation of gene expression by extracellular cyclic AMP.

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Global Down-Regulation of Gene Expression in the Brain Using RNA Interference, with Emphasis on Monoamine Transporters and GPCRs: Implications for Target Characterization in Psychiatric and Neurological Disorders

Journal of Receptors and Signal Transduction ◽

10.1080/10799890600929663 ◽

2006 ◽

Vol 26 (5-6) ◽

pp. 527-547 ◽

Cited By ~ 16

Author(s):

DANIEL HOYER ◽

DEEPAK R. THAKKER ◽

FRANÇOIS NATT ◽

RAINER MAIER ◽

DIETER HUESKEN ◽

...

Keyword(s):

Gene Expression ◽

Rna Interference ◽

Neurological Disorders ◽

Regulation Of Gene Expression ◽

Monoamine Transporters ◽

Down Regulation ◽

Target Characterization ◽

The Brain

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Estrogen Inhibition of Periosteal Bone Formation in Rat Long Bones: Down-Regulation of Gene Expression for Bone Matrix Proteins*

Endocrinology ◽

10.1210/endo-127-3-1346 ◽

1990 ◽

Vol 127 (3) ◽

pp. 1346-1351 ◽

Cited By ~ 80

Author(s):

RUSSELL T. TURNER ◽

DOUGLAS S. COLVARD ◽

THOMAS C. SPELSBERG

Keyword(s):

Gene Expression ◽

Bone Formation ◽

Bone Matrix ◽

Regulation Of Gene Expression ◽

Matrix Proteins ◽

Long Bones ◽

Down Regulation ◽

Periosteal Bone Formation ◽

Bone Matrix Proteins

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Down-Regulation of Gene Expression in Mammalian Systems via siRNA Technology

Gene Biotechnology ◽

10.1201/b10919-25 ◽

2016 ◽

pp. 487-500

Keyword(s):

Gene Expression ◽

Regulation Of Gene Expression ◽

Down Regulation

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Transcriptional profiling reveals divergent roles of PPARα and PPARβ/δ in regulation of gene expression in mouse liver

Physiological Genomics ◽

10.1152/physiolgenomics.00127.2009 ◽

2010 ◽

Vol 41 (1) ◽

pp. 42-52 ◽

Cited By ~ 80

Author(s):

Linda M. Sanderson ◽

Mark V. Boekschoten ◽

Beatrice Desvergne ◽

Michael Müller ◽

Sander Kersten

Keyword(s):

Gene Expression ◽

Mouse Liver ◽

Target Genes ◽

Glucose Utilization ◽

Plasma Cholesterol ◽

Transcriptional Profiling ◽

Regulation Of Gene Expression ◽

Lipoprotein Metabolism ◽

Peroxisome Proliferator ◽

Fed State

Little is known about the role of the transcription factor peroxisome proliferator-activated receptor (PPAR) β/δ in liver. Here we set out to better elucidate the function of PPARβ/δ in liver by comparing the effect of PPARα and PPARβ/δ deletion using whole genome transcriptional profiling and analysis of plasma and liver metabolites. In fed state, the number of genes altered by PPARα and PPARβ/δ deletion was similar, whereas in fasted state the effect of PPARα deletion was much more pronounced, consistent with the pattern of gene expression of PPARα and PPARβ/δ. Minor overlap was found between PPARα- and PPARβ/δ-dependent gene regulation in liver. Pathways upregulated by PPARβ/δ deletion were connected to innate immunity and inflammation. Pathways downregulated by PPARβ/δ deletion included lipoprotein metabolism and various pathways related to glucose utilization, which correlated with elevated plasma glucose and triglycerides and reduced plasma cholesterol in PPARβ/δ−/− mice. Downregulated genes that may underlie these metabolic alterations included Pklr, Fbp1, Apoa4, Vldlr, Lipg, and Pcsk9, which may represent novel PPARβ/δ target genes. In contrast to PPARα−/− mice, no changes in plasma free fatty acid, plasma β-hydroxybutyrate, liver triglycerides, and liver glycogen were observed in PPARβ/δ−/− mice. Our data indicate that PPARβ/δ governs glucose utilization and lipoprotein metabolism and has an important anti-inflammatory role in liver. Overall, our analysis reveals divergent roles of PPARα and PPARβ/δ in regulation of gene expression in mouse liver.

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Shared up-regulation and contrasting down-regulation of gene expression distinguish desiccation-tolerant from intolerant green algae

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1906904117 ◽

2020 ◽

Vol 117 (29) ◽

pp. 17438-17445

Author(s):

Elena L. Peredo ◽

Zoe G. Cardon

Keyword(s):

Gene Expression ◽

Green Algae ◽

Desiccation Tolerance ◽

Time Course ◽

Regulation Of Gene Expression ◽

Late Embryogenesis Abundant ◽

Down Regulation ◽

Regulation Of Expression ◽

Active Growth ◽

Protective Genes

Among green plants, desiccation tolerance is common in seeds and spores but rare in leaves and other vegetative green tissues. Over the last two decades, genes have been identified whose expression is induced by desiccation in diverse, desiccation-tolerant (DT) taxa, including, e.g., late embryogenesis abundant proteins (LEA) and reactive oxygen species scavengers. This up-regulation is observed in DT resurrection plants, mosses, and green algae most closely related to these Embryophytes. Here we test whether this same suite of protective genes is up-regulated during desiccation in even more distantly related DT green algae, and, importantly, whether that up-regulation is unique to DT algae or also occurs in a desiccation-intolerant relative. We used three closely related aquatic and desert-derived green microalgae in the family Scenedesmaceae and capitalized on extraordinary desiccation tolerance in two of the species, contrasting with desiccation intolerance in the third. We found that during desiccation, all three species increased expression of common protective genes. The feature distinguishing gene expression in DT algae, however, was extensive down-regulation of gene expression associated with diverse metabolic processes during the desiccation time course, suggesting a switch from active growth to energy-saving metabolism. This widespread downshift did not occur in the desiccation-intolerant taxon. These results show that desiccation-induced up-regulation of expression of protective genes may be necessary but is not sufficient to confer desiccation tolerance. The data also suggest that desiccation tolerance may require induced protective mechanisms operating in concert with massive down-regulation of gene expression controlling numerous other aspects of metabolism.

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Transcriptional profiling of a Staphylococcus aureus clinical isolate and its isogenic agr and sarA mutants reveals global differences in comparison to the laboratory strain RN6390

Microbiology ◽

10.1099/mic.0.29033-0 ◽

2006 ◽

Vol 152 (10) ◽

pp. 3075-3090 ◽

Cited By ~ 111

Author(s):

James Cassat ◽

Paul M. Dunman ◽

Ellen Murphy ◽

Steven J. Projan ◽

Karen E. Beenken ◽

...

Keyword(s):

Gene Expression ◽

Staphylococcus Aureus ◽

Clinical Isolate ◽

Biofilm Formation ◽

Regulatory Networks ◽

Transcriptional Profiling ◽

Expression Patterns ◽

Regulation Of Gene Expression ◽

Laboratory Strain ◽

Transcriptional Profile

The production of Staphylococcus aureus virulence factors is under the control of complex regulatory circuits. Most studies aimed at defining these regulatory networks have focused on derivatives of the strain NCTC 8325, most notably RN6390. However, all NCTC 8325 derivatives, including RN6390, possess an 11 bp deletion in rsbU. This deletion renders NCTC 8325 derivatives naturally sigma-factor-B deficient. Recent studies have shown that RN6390 is also deficient, in comparison to clinical isolates, with respect to biofilm formation, a process which is important for both pathogenesis and antimicrobial resistance. Based on these considerations, the authors carried out genome-scale transcriptional profiling, comparing RN6390 with the virulent rsbU-positive clinical isolate UAMS-1. The results revealed significant genome-wide differences in expression patterns between RN6390 and UAMS-1, and suggested that the overall transcriptional profile of UAMS-1 is geared toward expression of factors that promote colonization and biofilm formation. In contrast, the transcriptional profile of RN6390 was heavily influenced by RNAIII expression, resulting in a phenotype characterized by increased production of exoproteins, and decreased capacity to form a biofilm. The greater influence of agr in RN6390 relative to UAMS-1 was also evident when the transcriptional profile of UAMS-1 was compared with that of its isogenic sarA and agr mutants. Specifically, the results indicate that, in contrast to NCTC 8325 derivatives, agr plays a limited role in overall regulation of gene expression in UAMS-1, when compared with sarA. Furthermore, by defining the sarA regulon in a biofilm-positive clinical isolate, and comparing the results with transcriptional profiling experiments defining biofilm-associated gene expression patterns in the same strain, the authors identified a sarA-regulated operon (alsSD) that is also induced in biofilms, and demonstrated that mutation of alsSD results in reduced capacity to form a biofilm.

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Global Suppression of the Host Antiviral Response by Ebola- and Marburgviruses: Increased Antagonism of the Type I Interferon Response Is Associated with Enhanced Virulence

Journal of Virology ◽

10.1128/jvi.80.6.3009-3020.2006 ◽

2006 ◽

Vol 80 (6) ◽

pp. 3009-3020 ◽

Cited By ~ 126

Author(s):

John C. Kash ◽

Elke Mühlberger ◽

Victoria Carter ◽

Melanie Grosch ◽

Olivia Perwitasari ◽

...

Keyword(s):

Gene Expression ◽

Acute Phase Proteins ◽

Transcriptional Profiling ◽

Regulation Of Gene Expression ◽

Interferon Response ◽

Type I ◽

Type I Ifn ◽

Cell Gene Expression ◽

Infected Cells ◽

Immune Related Genes

ABSTRACT We studied the effect of filovirus infection on host cell gene expression by characterizing the regulation of gene expression responses in human liver cells infected with Zaire Ebolavirus (ZEBOV), Reston Ebolavirus (REBOV), and Marburgvirus (MARV), using transcriptional profiling and bioinformatics. Expression microarray analysis demonstrated that filovirus infection resulted in the up-regulation of immune-related genes and the down-regulation of many coagulation and acute-phase proteins. These studies further revealed that a common feature of filovirus virulence is suppression of key cellular antiviral responses, including TLR-, interferon (IFN) regulatory factor 3-, and PKR-related pathways. We further showed that ZEBOV and MARV were more potent antagonists of the IFN response and inhibited the expression of most of the IFN-stimulated genes (ISGs) observed in mock-infected IFN-α-2b treated cells, compared to REBOV infection, which activated more than 20% of these ISGs. Finally, we examined IFN-related gene expression in filovirus-infected cells treated with IFN-α-2b. These experiments revealed that a majority of genes induced in mock-infected cells treated with type I IFN were antagonized in treated ZEBOV- and MARV-infected cells, while in contrast, REBOV infection resulted in a significant increase in ISG expression. Analysis of STAT1 and -2 phosphorylation following IFN treatment showed a significant reduction of STAT phosphorylation for MARV but not for ZEBOV and REBOV, indicating that different mechanisms might be involved in antagonizing IFN signaling pathways by the different filovirus species. Taken together, these studies showed a correlation between antagonism of type I IFN responses and filovirus virulence.

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