scholarly journals Dissecting the membrane-microtubule sensor in grapevine defence

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Pingyin Guan ◽  
Wenjing Shi ◽  
Michael Riemann ◽  
Peter Nick
Keyword(s):  
Gene Expression ◽  
Experimental System ◽  
Inhibitory Effect ◽  
Perception System ◽  
Diphenylene Iodonium ◽  
Plant Microtubules ◽  
Defence Responses ◽  
Stress Signals ◽  
Basal Immunity

AbstractSpecific populations of plant microtubules cooperate with the plasma membrane to sense and process abiotic stress signals, such as cold stress. The current study derived from the question, to what extent this perception system is active in biotic stress signalling. The experimental system consisted of grapevine cell lines, where microtubules or actin filaments are visualised by GFP, such that their response became visible in vivo. We used the bacterial elicitors harpin (inducing cell-death related defence), or flg22 (inducing basal immunity) in combination with modulators of membrane fluidity, or microtubules. We show that DMSO, a membrane rigidifier, can cause microtubule bundling and trigger defence responses, including activation of phytoalexin transcripts. However, DMSO inhibited the gene expression in response to harpin, while promoting the gene expression in response to flg22. Treatment with DMSO also rendered microtubules more persistent to harpin. Paradoxically, Benzylalcohol (BA), a membrane fluidiser, acted in the same way as DMSO. Neither GdCl3, nor diphenylene iodonium were able to block the inhibitory effect of membrane rigidification on harpin-induced gene expression. Treatment with taxol stabilised microtubule against harpin but amplified the response of PAL transcripts. Therefore, the data support implications of a model that deploys specific responses to pathogen-derived signals.

An in vivo whole-plant experimental system for the analysis of gene expression in extraradical mycorrhizal mycelium

Mycorrhiza ◽  
2017 ◽  
Vol 27 (7) ◽  
pp. 659-668 ◽  
Author(s):  
Alessandra Pepe ◽  
Cristiana Sbrana ◽  
Nuria Ferrol ◽  
Manuela Giovannetti
Keyword(s):  
Gene Expression ◽  
Experimental System ◽  
Whole Plant

scholarly journals Differentiation of T cell lymphokine gene expression: the in vitro acquisition of T cell memory.

1991 ◽  
Vol 173 (1) ◽  
pp. 25-36 ◽  
Author(s):  
S Ehlers ◽  
K A Smith
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
T Cell ◽  
Interleukin 2 ◽  
Experimental System ◽  
Functional Differentiation ◽  
Gene Repertoire ◽  
Anamnestic Response

A simple in vitro experimental system was devised to reflect the in vivo generation of a T cell anamnestic response so that T cell differentiation could be examined at the level of lymphokine gene expression. Comparison of neonatal and adult T cells revealed that both populations expressed the genes for interleukin 2 (IL-2) and its receptor, but only adult T cells were capable of transcribing mRNAs for IL-3, IL-4, IL-5, IL-6, interferon gamma, and granulocyte/macrophage colony-stimulating factor. However, neonatal T cells could be induced to undergo functional differentiation in vitro, thereby acquiring the capacity to express the lymphokine gene repertoire characteristic for adult T cells. These data suggest that the T cells generated from neonatal blood by a primary stimulation in vitro are functionally indistinguishable from the T cells in adult blood that presumably have undergone primary stimulation in vivo. Therefore, we propose that the term "memory cell" be applied to those T cells that can be identified by their differentiated state of inducible effector-lymphokine gene expression.

17β-Estradiol inhibits cyclic strain-induced endothelin-1 gene expression within vascular endothelial cells

2004 ◽  
Vol 287 (3) ◽  
pp. H1254-H1261 ◽  
Author(s):  
Shu-Hui Juan ◽  
Jin-Jer Chen ◽  
Cheng-Hsien Chen ◽  
Heng Lin ◽  
Ching-Feng Cheng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Cyclic Strain ◽  
Inhibitory Effect ◽  
Ros Generation ◽  
Cardiovascular Tissue ◽  
Erk Phosphorylation ◽  
Diphenylene Iodonium ◽  
17Β Estradiol

It has been well documented previously that 17β-estradiol (E2) exerts a protective effect on cardiovascular tissue. The possible role of E2 in the regulation of endothelin (ET)-1 production has been previously reported, although the complex mechanisms by which E2 inhibits ET-1 expression are not completely understood. The aims of this study were to examine whether E2 was able to alter strain-induced ET-1 gene expression and also to identify the putative underlying signaling pathways that exist within endothelial cells. For cultured endothelial cells, E2 (1–100 nM), but not 17α-estradiol, inhibited the level of strain-induced ET-1 gene expression and also peptide secretion. This inhibitory effect elicited by E2 was able to be prevented by the coincubation of endothelial cells with the estrogen receptor antagonist ICI-182,780 (1 μM). E2 also inhibited strain-enhanced NADPH oxidase activity and intracellular reactive oxygen species (ROS) generation as measured by the redox-sensitive fluorescent dye 2′,7′-dichlorofluorescin diacetate and the level of extracellular signal-regulated kinase (ERK) phosphorylation. Furthermore, the presence of E2 and antioxidants such as N-acetylcysteine and diphenylene iodonium were able to elicit a decrease in the level of strain-induced ET-1 secretion, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1 binding activity. In summary, we demonstrated, for the first time, that E2 inhibits strain-induced ET-1 gene expression, partially by interfering with the ERK pathway via the attenuation of strain-induced ROS generation. Thus this study delivers important new insight regarding the molecular pathways that may contribute to the proposed beneficial effects of estrogen on the cardiovascular system.

scholarly journals Molecular competition can shape enhancer activity in the Drosophila embryo

2021 ◽  
Author(s):  
Rachel Waymack ◽  
Mario Gad ◽  
Zeba Wunderlich
Keyword(s):  
Gene Expression ◽  
Binding Sites ◽  
Inhibitory Effect ◽  
Drosophila Embryo ◽  
Enhancer Activity ◽  
Endogenous Gene ◽  
Endogenous Genes ◽  
Regulatory Dna ◽  
The Impact

Transgenic reporters allow the measurement of regulatory DNA activity in vivo and consequently have long been useful tools in the study of enhancers. Despite the utility of transgenic reporters, few studies have investigated the potential effects these reporters have on the expression of other transgenic reporters or endogenous genes. A full understanding of the impacts transgenic reporters have on expression is required for accurate interpretation of transgenic reporter data and characterization of gene regulatory mechanisms. Here, we investigate the impact transgenic reporters have on the expression of other transgenic reporters and endogenous genes. By measuring the expression of Kruppel (Kr) enhancer reporters in live Drosophila embryos that contain either one or two copies of identical reporters, we find reporters have an inhibitory effect on one another's expression. Further, expression of a nearby endogenous gene is decreased in the presence of a Kr enhancer reporter. Through the use of competitor binding site arrays, we present evidence that reporters, and potentially endogenous genes, are competing for transcription factors (TFs). Increasing the number of competitor Bcd binding sites decreases the peak levels and spatial extent of Bcd-regulated enhancer reporters' expression. To understand how small numbers of added TF binding sites could impact gene expression to the extent we observe, we develop a simple thermodynamic model of our system. Our model predicts competition of the measured magnitude specifically if TF binding is restricted to distinct nuclear subregions, underlining the importance of the non-homogenous nature of the nucleus in regulating gene expression.

Melatonin Differentially Modulates NF-кB Expression in Breast and Liver Cancer Cells

2019 ◽  
Vol 18 (12) ◽  
pp. 1688-1694 ◽  
Author(s):  
Jucimara Colombo ◽  
Bruna V. Jardim-Perassi ◽  
João P.S. Ferreira ◽  
Cristine Z. Braga ◽  
Nathália M. Sonehara ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Transcription Factor ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Hepg2 Cells ◽  
In Vitro Study ◽  
Inhibitory Effect

Background: NF-kB (nuclear factor kappa B) is a transcription factor composed of two subunits, p50 and p65, which plays a key role in the inflammatory process. Melatonin has oncostatic, antiangiogenic and antimetastatic properties, and some recent studies have indicated an inhibitory effect of melatonin on NF-kB in some types of cancer. This work aims to investigate the effects of melatonin treatment on the expression of NFkB in breast and liver cancer models. Method: The breast cancer xenographic model was performed using female Balb/c nude athymic mice injected with MDA-MB-231 cells. The animals were treated with 40 mg/Kg of melatonin for 21 days. Volume of the tumors was measured with a digital caliper. Hepatocarcinoma model was developed by using the HepG2 cells in vitro, treated with 1 mM melatonin for 24 h. The expression of NF-kB protein was verified by immunohistochemistry and immunocytochemistry and quantified by optical densitometry, in vivo study and in vitro study, respectively. NF-kB gene expression was performed by quantitative RT-PCR. Results: The breast cancer xenografts nude mice treated with melatonin showed reduced tumor size (P=0.0022). There was a decrease in NF-kB protein staining (P=0.0027) and gene expression (P=0.0185) in mice treated with melatonin. The opposite results were observed for the hepatocarcinoma model. HepG2 cells treated with melatonin showed an increase in the NF-kB immunostaining when compared to control cells (P=0.0042). Conclusion: Our results indicated that the treatment with melatonin was able to decrease both gene and protein expressions of NF-kB in breast cancer cells and, conversely, increase the transcription factor protein expression in hepatocarcinoma cells. These data highlighted a double role in the expression of NF-kB, depending on the cell type. Further studies are needed to better elucidate the action of melatonin in NF-kB, since this transcription factor acts on different signaling pathways that are fundamental for carcinogenesis.

Cobalt exerts opposite effects on erythropoietin gene expression in rat hepatocytes in vivo and in vitro

1995 ◽  
Vol 269 (5) ◽  
pp. R995-R1001
Author(s):  
T. Gopfert ◽  
K. U. Eckardt ◽  
B. Gess ◽  
A. Kurtz
Keyword(s):  
Gene Expression ◽  
Oxygen Sensor ◽  
Rat Hepatocytes ◽  
Inhibitory Effect ◽  
Ribonuclease Protection Assay ◽  
Mrna Levels ◽  
Adult Rats ◽  
Ribonuclease Protection

This study investigates the effects of hypoxia and of cobalt on erythropoietin (EPO) gene expression in hepatocytes in vivo and in vitro in neonatal, juvenile, and adult rats. With the use of the ribonuclease protection assay to quantify RNA, both hypoxia (0.1% CO or 9% O2) and cobalt (60 mg/kg) elicit production of increased amounts of EPO mRNA in neonatal and juvenile rat liver in vivo. In vitro hepatocyte EPO gene expression could be reproducibly stimulated by hypoxia (3% O2) but not by cobaltous chloride (50-150 microM) within 2-20 h. Conversely, cobalt substantially attenuated the rise of EPO mRNA levels in response to hypoxia. This inhibitory effect of cobalt was mimicked by zinc but not by other metals. CO attenuated the rise of EPO mRNA levels in vitro in response to hypoxia; this inhibitory effect coincided with an inhibition of total RNA synthesis as determined by [3H]uridine incorporation. The lack of specific inhibitory effects of CO and of specific stimulatory effects of cobalt on hepatocyte EPO gene expression in vitro suggests that a specific heme oxygen sensor may be less important than in hepatoma cells.

scholarly journals A Purified Capsular Polysaccharide Markedly Inhibits Inflammatory Response during Endotoxic Shock

2012 ◽  
Vol 81 (1) ◽  
pp. 90-98 ◽  
Author(s):  
M. Piccioni ◽  
C. Monari ◽  
S. Kenno ◽  
E. Pericolini ◽  
E. Gabrielli ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Capsular Polysaccharide ◽  
Endotoxic Shock ◽  
Experimental System ◽  
Inhibitory Effect ◽  
Necrosis Factor Alpha ◽  
Content Type ◽  
Tnf Α ◽  
Factor Alpha

Capsular material of the opportunistic fungusCryptococcus neoformansis composed mainly of a polysaccharide named glucuronoxylomannan (GXM). In this study, the effects of GXM were analyzed in anin vivoexperimental system of lipopolysaccharide (LPS)-induced shock. Endotoxic shock was induced in mice by a single intraperitoneal injection of LPS fromEscherichia coli. GXM treatment reduced the mortality of mice at early stages. Mice treated with LPS alone showed markedly increased plasma levels of tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and IL-6, whereas mice that were also treated with GXM showed significantly lower plasma levels of these cytokines. This effect was related to a marked suppression of Akt and IκBα activation. Importantly, the inhibitory effect of GXM on proinflammatory cytokine secretion was reproduced by treatment with wortmannin, an inhibitor of the Akt transcription pathway. Our results indicate that GXM has a beneficial effect on endotoxic shock, resulting in a significant increase in the rate of survival by dampening the hyperinflammatory response.

scholarly journals PRMT5 Inhibition Promotes PD-L1 Expression and Immuno-Resistance in Lung Cancer

2022 ◽  
Vol 12 ◽  
Author(s):  
Rui Hu ◽  
Bingqian Zhou ◽  
Zheyi Chen ◽  
Shiyu Chen ◽  
Ningdai Chen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Lung Cancer ◽  
Tumor Cell ◽  
Lung Tumor ◽  
Inhibitory Effect ◽  
Immunocompetent Mice ◽  
Immunocompromised Mice ◽  
Cell Expression

Protein arginine transferase 5 (PRMT5) has been implicated as an important modulator of tumorigenesis as it promotes tumor cell proliferation, invasion, and metastasis. Studies have largely focused on PRMT5 regulating intrinsic changes in tumors; however, the effects of PRMT5 on the tumor microenvironment and particularly immune cells are largely unknown. Here we found that targeting PRMT5 by genetic or pharmacological inhibition reduced lung tumor progression in immunocompromised mice; however, the effects were weakened in immunocompetent mice. PRMT5 inhibition not only decreased tumor cell survival but also increased the tumor cell expression of CD274 in vitro and in vivo, which activated the PD1/PD-L1 axis and eliminated CD8+T cell antitumor immunity. Mechanistically, PRMT5 regulated CD274 gene expression through symmetric dimethylation of histone H4R3, increased deposition of H3R4me2s on CD274 promoter loci, and inhibition of CD274 gene expression. Targeting PRMT5 reduced this inhibitory effect and promoted CD274 expression in lung cancer. However, PRMT5 inhibitors represent a double-edged sword as they may selectively kill cancer cells but may also disrupt the antitumor immune response. The combination of PRMT5 inhibition and ani-PD-L1 therapy resulted in an increase in the number and enhanced the function of tumor-infiltrating T cells. Our findings address an unmet clinical need in which combining PRMT5 inhibition with anti-PD-L1 therapy could be a promising strategy for lung cancer treatment.

scholarly journals CDK19 is a Regulator of Triple-Negative Breast Cancer Growth

2018 ◽  
Author(s):  
Robert W. Hsieh ◽  
Angera H. Kuo ◽  
Ferenc A. Scheeren ◽  
Mark A. Zarnegar ◽  
Shaheen S. Sikandar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Triple Negative Breast Cancer ◽  
Therapeutic Target ◽  
Triple Negative ◽  
Mammary Epithelial Cells ◽  
Inhibitory Effect ◽  
Mammary Epithelial

AbstractTriple-negative breast cancer (TNBC) is a poor prognosis disease with no clinically approved targeted therapies. Here, using in vitro and in vivo RNA interference (RNAi) screens in TNBC patient-derived xenografts (PDX), we identify cyclin dependent kinase 19 (CDK19) as a potential therapeutic target. Using in vitro and in vivo TNBC PDX models, we validated the inhibitory effect of CDK19 knockdown on tumor initiation, proliferation and metastases. Despite this, CDK19 knockdown did not affect the growth of non-transformed mammary epithelial cells. Using CD10 and EpCAM as novel tumor initiating cell (TIC) markers, we found the EpCAMmed/high/CD10−/low TIC sub-population to be enriched in CDK19 and a putative cellular target of CDK19 inhibition. Comparative gene expression analysis of CDK19 and CDK8 knockdowns revealed that CDK19 regulates a number of cancer-relevant pathways, uniquely through its own action and others in common with CDK8. Furthermore, although it is known that CDK19 can act at enhancers, our CHIP-Seq studies showed that CDK19 can also epigenetically modulate specific H3K27Ac enhancer signals which correlate with gene expression changes. Finally, to assess the potential therapeutic utility of CDK19, we showed that both CDK19 knockdown and chemical inhibition of CDK19 kinase activity impaired the growth of pre-established PDX tumors in vivo. Current strategies inhibiting transcriptional co-factors and targeting TICs have been limited by toxicity to normal cells. Because of CDK19’s limited tissue distribution and the viability of CDK19 knockout mice, CDK19 represents a promising therapeutic target for TNBC.

scholarly journals Evidence for a transient inhibitory effect of insulin on GLUT2 expression in the liver: studies in vivo and in vitro

1993 ◽  
Vol 293 (1) ◽  
pp. 119-124 ◽  
Author(s):  
C Postic ◽  
R Burcelin ◽  
F Rencurel ◽  
J P Pegorier ◽  
M Loizeau ◽  
...  
Keyword(s):  
Gene Expression ◽  
Glucose Transporter ◽  
Primary Cultures ◽  
Rat Hepatocytes ◽  
Inhibitory Effect ◽  
Mrna Concentration ◽  
Glut2 Gene ◽  
Effect Of Glucose

The glucose transporter GLUT2 is expressed predominantly in the liver. Previous studies have shown that glucose increases GLUT2 mRNA concentration in primary cultures of rat hepatocytes. Since insulin controls the glucose metabolism in the liver, it could be involved in the regulation of GLUT2 gene expression. In vivo, hyperinsulinaemia induced a transient inhibitory effect on liver GLUT2 gene expression, the maximal inhibition of GLUT2 mRNA concentration (93 +/- 6%) being observed after 6 h. When hyperglycaemia was associated with hyperinsulinaemia, the decrease in liver GLUT2 mRNA concentration was partially prevented. The respective effects of glucose and insulin were studied in vitro by primary culture of rat hepatocytes. Insulin alone exerted a transient inhibitory effect on GLUT2 mRNA concentration. When insulin and glucose (10-20 mM) were associated, the stimulatory effect of glucose on GLUT2 gene expression was predominant. In conclusion, the present study shows that GLUT2 mRNA concentration was conversely regulated by insulin and glucose, both in vitro and in vivo.

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