scholarly journals Gene Expression by the Sulfate-Reducing Bacterium Desulfovibrio vulgaris Hildenborough Grown on an Iron Electrode under Cathodic Protection Conditions

2008 ◽  
Vol 74 (8) ◽  
pp. 2404-2413 ◽  
Author(s):  
Sean M. Caffrey ◽  
Hyung Soo Park ◽  
Jenny Been ◽  
Paul Gordon ◽  
Christoph W. Sensen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Cathodic Protection ◽  
Gaseous Hydrogen ◽  
Iron Electrode ◽  
Desulfovibrio Vulgaris ◽  
Wild Type ◽  
Sulfate Reducing ◽  
Genes Encoding

ABSTRACT The genome sequence of the sulfate-reducing bacterium Desulfovibrio vulgaris Hildenborough was reanalyzed to design unique 70-mer oligonucleotide probes against 2,824 probable protein-coding regions. These included three genes not previously annotated, including one that encodes a c-type cytochrome. Using microarrays printed with these 70-mer probes, we analyzed the gene expression profile of wild-type D. vulgaris grown on cathodic hydrogen, generated at an iron electrode surface with an imposed negative potential of −1.1 V (cathodic protection conditions). The gene expression profile of cells grown on cathodic hydrogen was compared to that of cells grown with gaseous hydrogen bubbling through the culture. Relative to the latter, the electrode-grown cells overexpressed two hydrogenases, the hyn-1 genes for [NiFe] hydrogenase 1 and the hyd genes, encoding [Fe] hydrogenase. The hmc genes for the high-molecular-weight cytochrome complex, which allows electron flow from the hydrogenases across the cytoplasmic membrane, were also overexpressed. In contrast, cells grown on gaseous hydrogen overexpressed the hys genes for [NiFeSe] hydrogenase. Cells growing on the electrode also overexpressed genes encoding proteins which promote biofilm formation. Although the gene expression profiles for these two modes of growth were distinct, they were more closely related to each other than to that for cells grown in a lactate- and sulfate-containing medium. Electrochemically measured corrosion rates were lower for iron electrodes covered with hyn-1, hyd, and hmc mutant biofilms than for wild-type biofilms. This confirms the importance, suggested by the gene expression studies, of the corresponding gene products in D. vulgaris-mediated iron corrosion.

Wild-type and mutant α-synuclein induce a multi-component gene expression profile consistent with shared pathophysiology in different transgenic mouse models of PD

2007 ◽  
Vol 204 (1) ◽  
pp. 421-432 ◽  
Author(s):  
Renee M. Miller ◽  
Gretchen L. Kiser ◽  
Tamma Kaysser-Kranich ◽  
Cindy Casaceli ◽  
Emanuela Colla ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transgenic Mouse ◽  
Gene Expression Profile ◽  
Mouse Models ◽  
Expression Profile ◽  
Transgenic Mouse Models ◽  
Wild Type ◽  
Component Gene

scholarly journals Effect of mild restriction of food intake on gene expression profile in the liver of young rats: reference data for in vivo nutrigenomics study

2010 ◽  
Vol 104 (7) ◽  
pp. 941-950 ◽  
Author(s):  
Kenji Saito ◽  
Yutaka Ohta ◽  
Manabu Sami ◽  
Tomomasa Kanda ◽  
Hisanori Kato
Keyword(s):  
Gene Expression ◽  
Food Intake ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Fatty Acid Synthase ◽  
Reference Data ◽  
Global Gene Expression ◽  
Energy Restriction ◽  
Genes Encoding

Recent transcriptomics studies on the effect of long-term or severe energy restriction (ER) have revealed that many genes are dynamically modulated by this condition in rodents. The present study was conducted to define the global gene expression profile in response to mild ER treatment. Growing rats were fed with reduced amount of diet (5–30 % ER) for 1 week or 1 month. Using DNA microarray analysis of the liver, seventy-two genes that were consistently changed through the different ER levels were identified. Many were related to lipid metabolism including genes encoding key enzymes such as carnitine palmitoyltransferase 1 and fatty acid synthase. Interestingly, a number of genes were altered even by 5 % ER for 1 week where no differences in weight gain were observed. The information obtained in the present study can be used as a valuable reference data source in the transcriptomics studies of food and nutrition in which subtle differences in food intake sometimes hinder appropriate interpretation of the data.

The Interaction of MOZ-TIF2 with Histone Chaperon Proteins CAF-1A and Asf1b Alters MOZ Regulated Gene Expression.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2208-2208
Author(s):  
Hong Yin ◽  
Jonathan Glass ◽  
Kerry L. Blanchard
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Global Gene Expression ◽  
Chromatin Assembly ◽  
Wild Type ◽  
Terminal Portion ◽  
Hek 293 ◽  
Assembly Factors ◽  
Regulated Gene Expression

Abstract We have identified a MOZ-TIF2 (MT2) fusion gene containing the N-terminal portion of MOZ and the C-terminal portion of TIF2 from a patient with acute leukemia with a chromosome 8 translocation. We report here that MOZ portion of MOZ-TIF2 associates with chromatin assembly factors, CAF1 (chromatin assembly factor 1) and ASF1 (anti-silencing factor 1) in mammalian cells. Both proteins not only bring histones to newly synthesized DNA to create chromatin structure in the replication of chromosomes and DNA damage-repair processes but also contribute to regulation of global gene expression. Using the MOZ portion of MT2 as the bait in the yeast two hybrid system, we found that the MOZ portion interacted with CAF1A and Asf1b. The interactions were further verified with GST-pull down experiments. Interestingly, co-immunoprecipitation with whole cell extracts from HEK 293 cells transiently transfected with GFP fusions of MOZ, MT2, and TIF2 showed that only MOZ strongly co-precipitated with CAF1A while MT2 only weakly co-precipitated. In contrast to CAF1A, MT2 showed a 3-fold stronger binding to Asf1b than wild type MOZ in pull-down experiments using S-tagged Asf1b and EGFP-fusions of MOZ, MT2, and TIF2. Further analysis of the domains within the MOZ portion of MT2 responsible for the interaction of CAF1A and Asf1b with MT2 indicated that the binding of CAF1A predominately depended on the PHD domain of MOZ and amino acids176–327 of CAF1A. The MYST domain of MOZ was responsible for the binding of the MOZ portion of MT2 to Asf1b. To further verify the differential binding of MOZ and MT2 to CAF1A and Asf1b, we observed the co-localization of transiently expressed EGFP-MOZ and EGFP-MT2 with DsRed-CAF1A in HEK 293 and Hela cells. In the merged images the MOZ co-localization with CAF-1A was stronger than the colocalization of MT2 with CAF1A and MT2 colocalization with Asf1b was stronger than MOZ colocalization with Asf1b. The co-localization of MOZ and MT2 with CAF1A with Asf1b was seen both in interphase and metaphase of the cell cycle. During the interphase, the co-localizations appeared with chromatin DNA and during metaphase the co-localizations were separated from chromatin DNA. The later phenomenon was further demonstrated with G2/M phase reagent, nocodozole. These results suggest a differential function of MT2 interacting with two chromatin assembly factors compared to wild-type MOZ. In view of the regulation of global gene expression by CAF1A and Asf1b, we examined the gene expression profile in U937 cells stably expressing MT2. Compared to the expression profile of control cells stably transfected with pcDNA3 vector alone, MT2 caused a > 5-fold change in expression 181 genes (104 genes increasing and 77 genes decreasing expression) (p = 0.05). While overexpression of wild type MOZ also altered gene expression (>5-fold increase in 479 genes and >5-fold decrease in 118 genes) a differential gene expression signature was seen between MOZ and MT2. MT2 altered expression of 57% of the 597 MOZ regulated genes. Included in the genes that were either up or down-regulated by MT2 were genes involved in multiple cell functions such as signal transduction, cell response to stimulus, and development. These results suggest that MT2 fusion may interfere with the function of wild type MOZ in global gene expression during the development of myeloid cells by differential interaction with chromatin chaperon proteins and the altered global gene expression profile could contribute to leukemogenesis.

ERG Deletions Define a Novel Subtype of B-Progenitor Acute Lymphoblastic Leukemia.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 691-691 ◽  
Author(s):  
Charles G. Mullighan ◽  
Christopher B. Miller ◽  
Xiaoping Su ◽  
Ina Radtke ◽  
James Dalton ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Lymphoblastic Leukemia ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Lymphoblastic Leukemia ◽  
Luciferase Reporter ◽  
The Novel ◽  
Wild Type ◽  
Cytogenetic Abnormalities ◽  
Novel Gene

Abstract In a previous gene expression profiling study of acute lymphoblastic leukemia (ALL), we identified a novel subtype of B-progenitor ALL (4.9% of 284 cases) with a unique gene expression profile, aberrant expression of CD2 and the absence of recurring cytogenetic abnormalities (Cancer Cell2002;1:133). Efforts to identify rearrangement or mutation of many of the top-ranked genes in the novel expression signature failed to identify a causative lesion. To further investigate the genetic basis of this subtype, we performed integrated genomic analysis of 277 ALL cases. Affymetrix 250k Sty and Nsp SNP microarrays were used in all cases, and Affymetrix U133A gene expression profiles were obtained on 183 of the cases. Unsupervised clustering of gene expression data identified 16 cases of the novel subtype, including all of the 14 previously defined cases. Remarkably, focal mono-allelic deletions of the ETS family member ERG (v-ets erythroblastosis virus E26 oncogene homolog) were detected by genome-wide copy number analysis in 11/16 (69%) of the novel cases, but not in any other ALL subtype. Extensive analysis failed to reveal evidence of translocations involving the altered ERG allele, indicating that these are intragenic deletions limited to ERG. The ERG deletions involved a subset of exons (ERG isoform 1 exons 3–7 or 3–9) resulting in the expression of internally deleted ERG transcripts with altered reading frames predicted to produce a prematurely truncated N-terminal protein fragment. However, using an alternative translational start site 5′ to exon 10, the transcripts also encode a ∼28kDa C-terminal ERG fragment that contains the entire C-terminal ETS DNA-binding and transactivation domains, but lacks all N-terminal domains. Importantly, western blot analysis of primary leukemic blasts revealed expression of only the 28kDa C-terminal ERG protein, along with full length ERG expressed from the retained wild type allele. Remarkably, the C-terminal ERG protein was also detected in 4 of 5 novel ALL cases that lacked detectable ERG deletions, but not in any other ALL subtype. In luciferase reporter assays, this aberrant ERG protein acts as a competitive inhibitor of wild type ERG. Analysis of a second cohort of 35 B-progenitor ALL cases lacking recurring cytogenetic abnormalities identified two cases with ERG deletions and a third expressing the aberrant ERG protein, all of which had the novel gene expression profile. Sequencing of ERG in 252 ALL cases identified only one case with an ERG mutation that resulted in a frameshift in the ETS domain. This case did not share the novel signature nor express the aberrant C-terminal ERG protein. Finally, in an analysis of 37 acute leukemia cell lines, the B-progenitor ALL line NALM-6 was found to harbor a focal, internally truncating ERG deletion, expressed the aberrant ERG protein, and shared the novel gene expression profile, thus identifying it as a model of this novel ALL subtype. These data establish focal ERG deletions as the genetic lesion underlying a novel subtype of ALL, and have expanded the genetic mechanisms that lead to the dysregulation of ERG from chromosomal translocations that result in enhanced transcriptional activity, to deletions that generate dominant negative forms of the transcription factor.

scholarly journals Prognostic Significance of Expression of a Single MicroRNA,miR-181a, in Cytogenetically Normal Acute Myeloid Leukemia: A Cancer and Leukemia Group B Study

2010 ◽  
Vol 28 (36) ◽  
pp. 5257-5264 ◽  
Author(s):  
Sebastian Schwind ◽  
Kati Maharry ◽  
Michael D. Radmacher ◽  
Krzysztof Mrózek ◽  
Kelsi B. Holland ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Myeloid Leukemia ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Myeloid Leukemia ◽  
Prognostic Significance ◽  
Comprehensive Cancer Center ◽  
Wild Type ◽  
The Impact ◽  
Acute Myeloid

PurposeTo evaluate the prognostic significance of expression levels of a single microRNA, miR-181a, in the context of established molecular markers in cytogenetically normal acute myeloid leukemia (CN-AML), and to gain insight into the leukemogenic role of miR-181a.Patients and MethodsmiR-181a expression was measured in pretreatment marrow using Ohio State University Comprehensive Cancer Center version 3.0 arrays in 187 younger (< 60 years) adults with CN-AML. Presence of other molecular prognosticators was assessed centrally. A gene-expression profile associated with miR-181a expression was derived using microarrays and evaluated by Gene-Ontology analysis.ResultsHigher miR-181a expression associated with a higher complete remission (CR) rate (P = .04), longer overall survival (OS; P = .01) and a trend for longer disease-free survival (DFS; P = .09). The impact of miR-181a was most striking in poor molecular risk patients with FLT3-internal tandem duplication (FLT3-ITD) and/or NPM1 wild-type, where higher miR-181a expression associated with a higher CR rate (P = .009), and longer DFS (P < .001) and OS (P < .001). In multivariable analyses, higher miR-181a expression was significantly associated with better outcome, both in the whole patient cohort and in patients with FLT3-ITD and/or NPM1 wild-type. These results were also validated in an independent set of older (≥ 60 years) patients with CN-AML. A miR-181a-associated gene-expression profile was characterized by enrichment of genes usually involved in innate immunity.ConclusionTo our knowledge, we provide the first evidence that the expression of a single microRNA, miR-181a, is associated with clinical outcome of patients with CN-AML and may refine their molecular risk classification. Targeted treatments that increase endogenous levels of miR-181a might represent novel therapeutic strategies.

Genomics of cardiac remodeling in angiotensin II-treated wild-type and LOX-1-deficient mice

2010 ◽  
Vol 42 (1) ◽  
pp. 42-54 ◽  
Author(s):  
Bum-Yong Kang ◽  
Changping Hu ◽  
Sunhyo Ryu ◽  
Junaid A. Khan ◽  
Michela Biancolella ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Knockout Mice ◽  
Cardiac Remodeling ◽  
Oxidant Stress ◽  
Reactive Oxygen Species Generation ◽  
Cardiac Response ◽  
Ang Ii ◽  
Wild Type

We studied the gene expression profile during cardiac hypertrophy induced by angiotensin (ANG) II in wild-type mice and the influence of LOX-1 deletion on the gene expression profile. Wild-type and LOX-1 knockout mice were given saline or ANG II infusion for 4 wk. The saline-treated LOX-1 knockout mice showed upregulation of several genes including Ddx3y and Eif2s3y. ANG II infusion enhanced expression of genes known to be associated with cardiac remodeling, such as Agt, Ace, Timp4, Fstl, and Tnfrst12a, as well as oxidant stress-related genes Gnaq, Sos1, and Rac1. Some other strongly upregulated genes identified in this study have not been previously associated with LOX-1 deletion and/or hypertension. To confirm these observations with ANG II infusion and LOX-1 deletion, cultured HL-1 mouse cardiomyocytes were exposed to ANG II or transfected with pCI-neo/LOX-1, which resulted in severalfold increase in reactive oxygen species generation, upregulation of ANG II type 1 (AT1) receptor, and cardiomyocyte growth. Quantitative PCR analysis of these treated cardiomyocytes confirmed upregulation of many of the genes identified in the in vivo study. This study provides the first set of data on the gene expression profiling of cardiac tissue treated with ANG II and expands on the important role of LOX-1 in cardiac response to ANG II.

scholarly journals T Cells Help To Amplify Inflammatory Responses Induced by Salmonella enterica Serotype Typhimurium in the Intestinal Mucosa

2008 ◽  
Vol 76 (5) ◽  
pp. 2008-2017 ◽  
Author(s):  
Ivan Godinez ◽  
Takeshi Haneda ◽  
Manuela Raffatellu ◽  
Michael D. George ◽  
Tatiane A. Paixão ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Salmonella Enterica ◽  
Inflammatory Responses ◽  
Mrna Levels ◽  
Genes Encoding ◽  
Ifn Γ ◽  
Cecal Mucosa

ABSTRACT Salmonella enterica serotype Typhimurium causes an acute inflammatory reaction in the ceca of streptomycin-pretreated mice. We determined global changes in gene expression elicited by serotype Typhimurium in the cecal mucosa. The gene expression profile was dominated by T-cell-derived cytokines and genes whose expression is known to be induced by these cytokines. Markedly increased mRNA levels of genes encoding gamma interferon (IFN-γ), interleukin-22 (IL-22), and IL-17 were detected by quantitative real-time PCR. Furthermore, the mRNA levels of genes whose expression is induced by IFN-γ, IL-22, or IL-17, including genes encoding macrophage inflammatory protein 2 (MIP-2), inducible nitric oxide synthase (Nos2), lipocalin-2 (Lcn2), MIP-1α, MIP-1β, and keratinocyte-derived cytokine (KC), were also markedly increased. To assess the importance of T cells in orchestrating this proinflammatory gene expression profile, we depleted T cells by using a monoclonal antibody prior to investigating cecal inflammation caused by serotype Typhimurium in streptomycin-pretreated mice. Depletion of CD3+ T cells resulted in a dramatic reduction in gross pathology, a significantly reduced recruitment of neutrophils, and a marked reduction in mRNA levels of Ifn-γ, Il-22, Il-17, Nos2, Lcn2, and Kc. Our results suggest that T cells play an important role in amplifying inflammatory responses induced by serotype Typhimurium in the cecal mucosa.

scholarly journals Effect of Chronic Valproic Acid Treatment on Hepatic Gene Expression Profile inWfs1Knockout Mouse

PPAR Research ◽  
2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Marite Punapart ◽  
Mall Eltermaa ◽  
Julia Oflijan ◽  
Silva Sütt ◽  
Anne Must ◽  
...  
Keyword(s):  
Gene Expression ◽  
Valproic Acid ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Expression Profiles ◽  
Peroxisome Proliferator ◽  
Hepatic Gene Expression ◽  
Wild Type ◽  
Drug Induced

Valproic acid (VPA) is a widely used anticonvulsant and mood-stabilizing drug whose use is often associated with drug-induced weight gain. Treatment with VPA has been shown to upregulateWfs1expressionin vitro. Aim of the present study was to compare the effect of chronic VPA treatment in wild type (WT) andWfs1knockout (KO) mice on hepatic gene expression profile. Wild type,Wfs1heterozygous, and homozygous mice were treated with VPA for three months (300 mg/kg i.p. daily) and gene expression profiles in liver were evaluated using Affymetrix Mouse GeneChip 1.0 ST array. We identified 42 genes affected byWfs1genotype, 10 genes regulated by VPA treatment, and 9 genes whose regulation by VPA was dependent on genotype. Among the genes that were regulated differentially by VPA depending on genotype was peroxisome proliferator-activated receptor delta (Ppard), whose expression was upregulated in response to VPA treatment in WT, but not inWfs1KO mice. Thus, regulation ofPpardby VPA is dependent onWfs1genotype.

Renal medullary gene expression in aquaporin-1 null mice

2005 ◽  
Vol 288 (2) ◽  
pp. F315-F321 ◽  
Author(s):  
Matthew R. McReynolds ◽  
Katherine M. Taylor-Garcia ◽  
Kevin A. Greer ◽  
James B. Hoying ◽  
Heddwen L. Brooks
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Transforming Growth Factor ◽  
Lipocalin 2 ◽  
Wild Type ◽  
Analysis Model ◽  
Transforming Growth Factor Α ◽  
Aquaporin 1 ◽  
Aldolase B

Mice that lack the aquaporin-1 gene (AQP1) lack a functional countercurrent multiplier mechanism, fail to concentrate the inner medullary (IM) interstitium, and present with a urinary concentrating defect. In this study, we use DNA microarrays to identify the gene expression profile of the IM of AQP1 null mice and corresponding changes in gene expression resulting from a loss of a hypertonic medullary interstitium. An ANOVA analysis model, CARMA, was used to isolate the knockout effect while taking into account experimental variability associated with microarray studies. In this study 5,701 genes of the possible ∼12,000 genes on the array were included in the ANOVA; 531 genes were identified as demonstrating a >1.5-fold up- or downregulation between the wild-type and knockout groups. We randomly selected 35 genes for confirmation by real-time PCR, and 29 of the 35 genes were confirmed using this method. The overall pattern of gene expression in the AQP1 null mice was one of downregulation compared with gene expression in the renal medullas of the wild-type mice. Heat shock proteins 105 and 94, aldose reductase, adenylate kinase 2, aldolase B, aldehyde reductase 6, and p8 were decreased in the AQP1 null mice. Carboxylesterase 3, matrilin 2, lipocalin 2, and transforming growth factor-α were increased in IM of AQP1 null mice. In addition, we observed a loss of vasopressin type 2 receptor mRNA expression in renal medullas of the AQP1 null mice. Thus the loss of the hyperosmotic renal interstitium, due to a loss of the concentrating mechanism, drastically altered not only the phenotype of these animals but also their renal medullary gene expression profile.

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