scholarly journals Transcriptome Analysis Reveals the Gene Expression Changes in the Silkworm (Bombyx mori) in Response to Hydrogen Sulfide Exposure

Insects ◽  
2021 ◽  
Vol 12 (12) ◽  
pp. 1110
Author(s):  
Rui Zhang ◽  
Yu-Yao Cao ◽  
Juan Du ◽  
Kiran Thakur ◽  
Shun-Ming Tang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hydrogen Sulfide ◽  
Transcriptome Analysis ◽  
Fat Body ◽  
Tca Cycle ◽  
Transcriptional Level ◽  
Dependent Manner ◽  
Transport Pathway ◽  
Shell Weight ◽  
Study Gene Expression

Hydrogen sulfide (H2S) has been recognized for its beneficial influence on physiological alterations. The development (body weight) and economic characteristics (cocoon weight, cocoon shell ratio, and cocoon shell weight) of silkworms were increased after continuous 7.5 µM H2S treatment. In the present study, gene expression changes in the fat body of silkworms at the 5th instar larvae in response to the H2S were investigated through comparative transcriptome analysis. Moreover, the expression pattern of significant differentially expressed genes (DEGs) at the 5th instar larvae was confirmed by quantitative real-time PCR (qRT-PCR) after H2S exposure. A total of 1200 (DEGs) was identified, of which 977 DEGs were up-regulated and 223 DEGs were down-regulated. Most of the DEGs were involved in the transport pathway, cellular community, carbohydrate metabolism, and immune-associated signal transduction. The up regulated genes under H2S exposure were involved in endocytosis, glycolysis/gluconeogenesis, the citrate cycle (TCA cycle), and the synthesis of fibroin, while genes related to inflammation were down-regulated, indicating that H2S could promote energy metabolism, the transport pathway, silk synthesis, and inhibit inflammation in the silkworm. In addition, the expression levels of these genes were increased or decreased in a time-dependent manner during the 5th instar larvae. These results provided insight into the effects of H2S on silkworms at the transcriptional level and a substantial foundation for understanding H2S function.

scholarly journals Transcriptome analysis of the effect of AHR on productive and unproductive pathways of in vitro megakaryocytopoiesis

2021 ◽  
Author(s):  
Léa Malo ◽  
Valentin Do Sacramento ◽  
Christian Gachet ◽  
François Lanza ◽  
Henri de la Salle ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcriptome Analysis ◽  
Gene Expression Pattern ◽  
Cell Types ◽  
Dependent Manner ◽  
Noticeable Effect ◽  
Human Cd34 ◽  
Extracellular Matrix Components ◽  
Genetic Perturbations

Human CD34+ progenitors can be differentiated in vitro into proplatelet-producing megakaryocytes (MKs) within 17 days. During this time, four cell populations emerge, phenotypically defined as CD34+CD41+ on day 7 (D7) and CD34+CD41+CD9- on D10 and D14 - qualified as productive because they can differentiate into proplatelet-forming cells during the D14-D17 period - and CD34-CD41+ or CD34+CD41+CD9+ on day 10 - qualified as unproductive because they are unable to form proplatelets later. Coculture with mesenchymal stem cells, or the presence of the AHR antagonist SR1, boosts the productive pathway in two ways: firstly, it increases the yield of D10 and D14 CD34+CD41+CD9- cells and secondly, it greatly increases their ability to generate proplatelets; in contrast, SR1 has no noticeable effect on the unproductive cell types. A transcriptome analysis was performed to decipher the genetic basis of these properties. This work represents the first extensive description of the genetic perturbations which accompany the differentiation of CD34+ progenitors into mature MKs at a subpopulation level. It highlights a wide variety of biological changes modulated in a time-dependent manner and allows anyone, according to his/her interests, to focus on specific biological processes accompanying MK differentiation. For example, the modulation of the expression of genes associated with cell proliferation, lipid and cholesterol synthesis, extracellular matrix components, intercellular interacting receptors and MK and platelet functions reflected the chronological development of the productive cells and pointed to unsuspected pathways. Surprisingly, SR1 only affected the gene expression profile of D10 CD34+CD41+CD9- cells; thus, as compared to these cells and those present on D14, the poorly productive D10 CD34+CD41+CD9- cells obtained in the absence of SR1 and the two unproductive populations present on D10 displayed an intermediate gene expression pattern. In other words, the ability to generate proplatelets between D10 and D14 appeared to be linked to the capacity of SR1 to delay MK differentiation, meanwhile avoiding intermediate and inappropriate genetic perturbations. Paradoxically, the D14 CD34+CD41+CD9- cells obtained under SR1- or SR1+ conditions were virtually identical, raising the question as to whether their strong differences in terms of proplatelet production, in the absence of SR1 and between D14 and D17, are mediated by miRNAs or by memory post-translational regulatory mechanisms.

scholarly journals Hydrogen Sulfide Alleviates Senescence of Fresh-cut Apple by Regulating Antioxidant Defense System and Senescence-related Gene Expression

HortScience ◽  
2016 ◽  
Vol 51 (2) ◽  
pp. 152-158 ◽  
Author(s):  
Ji-Lian Zheng ◽  
Lan-Ying Hu ◽  
Kang-Di Hu ◽  
Jun Wu ◽  
Feng Yang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hydrogen Sulfide ◽  
Antioxidant Defense System ◽  
Guaiacol Peroxidase ◽  
Dependent Manner ◽  
Related Gene ◽  
Apple Slices ◽  
Apple Tissue ◽  
Fresh Cut ◽  
Postharvest Senescence

Hydrogen sulfide (H2S) has been identified as a multifunctional signaling molecule in plants. Here, we show that H2S delayed postharvest senescence of fresh-cut apples (Malus ×pumila) in a dose-dependent manner. Exogenous H2S application maintained significantly higher levels of ascorbic acid, flavonoids, total phenolics, reducing sugars and soluble proteins, and lower levels of free amino acids in apple slices compared with controls. Further investigations showed that H2S significantly reduced the accumulation of superoxide radicals, hydrogen peroxide (H2O2) and malondialdehyde (MDA). Apple fruits fumigated with H2S contained significantly higher activities of ascorbate peroxidase (APX), catalase (CAT), glutathione reductase (GR), guaiacol peroxidase (POD) and superoxide dismutase (SOD), and lower activities of lipoxygenase (LOX), phenylalanine ammonia lyase (PAL), polyphenol oxidase (PPO), and protease relative to controls. H2S also upregulated MdDHAR expression and downregulated the expression of MdLOX2, MdPG1, MdPPO, MdACO1, MdERS1, and MdETR1 in postharvest apple tissue. The present study indicates that H2S was involved in delaying postharvest senescence of apples by acting as an antioxidant and by regulating senescence-related gene expression.

scholarly journals Activin A Decreases glucagon and arx Gene Expression in α-Cell Lines

2007 ◽  
Vol 21 (1) ◽  
pp. 259-273 ◽  
Author(s):  
Aline Mamin ◽  
Jacques Philippe
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Human Islets ◽  
Activin A ◽  
Protein Product ◽  
Control Element ◽  
Transcriptional Level ◽  
Dependent Manner ◽  
Β Cells

Abstract Activin A is a potent growth and differentiation factor involved in development, differentiation, and physiological functions of the endocrine pancreas; it increases insulin and pax4 gene expression in β-cells and can induce transdifferentiation of the exocrine acinar cell line AR42J into insulin-producing cells. We show here that Activin A decreases glucagon gene expression in the α-cell lines InR1G9 and αTC1 in a dose- and time-dependent manner and that the effect is blocked by Follistatin. This effect is also observed in adult human islets. Glucagon gene expression is inhibited at the transcriptional level by the Smad signaling pathway through the G3 DNA control element. Furthermore, Activin A decreases cell proliferation of InR1G9 and αTC1 cells as well as cyclin D2 and arx gene expression, whose protein product Arx has been shown to be critical for α-cell differentiation. Overexpression of Arx in Activin A-treated InR1G9 cells does not prevent the decrease in glucagon gene expression but corrects the inhibition of cell proliferation, indicating that Arx mediates the Activin A effects on the cell cycle. We conclude that Activin A has opposite effects on α-cells compared with β-cells, a finding that may have relevance during pancreatic endocrine lineage specification and physiological function of the adult islets.

scholarly journals Antithyroid Drugs Inhibit Thyroid Hormone Receptor-Mediated Transcription

2007 ◽  
Vol 92 (3) ◽  
pp. 1066-1072 ◽  
Author(s):  
Kenji Moriyama ◽  
Tetsuya Tagami ◽  
Takeshi Usui ◽  
Mitsuhide Naruse ◽  
Takuo Nambu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Thyroid Hormone ◽  
Hormone Receptors ◽  
Thyroid Hormone Receptor ◽  
Transient Gene Expression ◽  
Antithyroid Drugs ◽  
Transcriptional Level ◽  
Dependent Manner ◽  
Peripheral Tissues

Abstract Context: Methimazole (MMI) and propylthiouracil (PTU) are widely used as antithyroid drugs (ATDs) for the treatment of Graves’ disease. Both MMI and PTU reduce thyroid hormone levels by several mechanisms, including inhibition of thyroid hormone synthesis and secretion. In addition, PTU decreases 5′-deiodination of T4 in peripheral tissues. ATDs may also interfere with T3 binding to nuclear thyroid hormone receptors (TRs). However, the effect of ATDs on the transcriptional activities of T3 mediated by TRs has not been studied. Objective: The present study was undertaken to determine whether ATDs have an effect on the gene transcription regulated by T3 and TRs in vitro. Methods: Transient gene expression experiments and GH secretion assays were performed. To elucidate possible mechanisms of the antagonistic action of ATDs, the interaction between TR and nuclear cofactors was examined. Results: In the transient gene expression experiments, both MMI and PTU significantly suppressed transcriptional activities mediated by the TR and T3 in a dose-dependent manner. In mammalian two-hybrid assays, both drugs recruited one of the nuclear corepressors, nuclear receptor corepressor, to the TR in the absence of T3. In addition, PTU dissociated nuclear coactivators, such as steroid receptor coactivator-1 and glucocorticoid receptor interacting protein-1, from the TR in the presence of T3. Finally, MMI decreased the GH release that was stimulated by T3. Conclusions: ATDs inhibit T3 action by recruitment of transcriptional corepressors and/or dissociation of coactivators. This is the first report to show that ATDs can modulate T3 action at the transcriptional level.

scholarly journals Regulatory interplay between RNase III and asRNAs in E. coli; the case of AsflhD and the master regulator of motility, flhDC

2021 ◽  
Author(s):  
Maxence Lejars ◽  
Joel CAILLET ◽  
Maude Guillier ◽  
Jacqueline A Plumbridge ◽  
Eliane HAJNSDORF
Keyword(s):  
Gene Expression ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Transcriptional Level ◽  
Dependent Manner ◽  
Rnase Iii ◽  
Master Regulator ◽  
E Coli ◽  
Genes Encoding ◽  
Rna Chaperones

In order to respond to ever-changing environmental cues, bacteria have evolved resilient regulatory mechanisms controlling gene expression. At the post-transcriptional level, this is achieved by a combination of RNA-binding proteins, such as ribonucleases (RNases) and RNA chaperones, and regulatory RNAs including antisense RNAs (asRNAs). AsRNAs bound to their complementary mRNA are primary targets for the double-strand-specific endoribonuclease, RNase III. By comparing primary and processed transcripts in an rnc strain, mutated for RNase III, and its isogenic wild type strain, we detected several asRNAs. We confirmed the existence of RNase III-sensitive asRNA for crp, ompR, phoP and flhD genes, encoding master regulators of gene expression. AsflhD, the asRNA to the master regulator of motility flhDC, is slightly induced under heat-shock conditions in a sigma24 (RpoE)-dependent manner. We demonstrate that expression of AsflhD asRNA is involved in the transcriptional attenuation of flhD and thus participates in the control of the whole motility cascade. This study demonstrates that AsflhD and RNase III are additional players in the complex regulation ensuring a tight control of flagella synthesis and motility.

scholarly journals LPS induces CD40 gene expression through the activation of NF-κB and STAT-1α in macrophages and microglia

Blood ◽  
2005 ◽  
Vol 106 (9) ◽  
pp. 3114-3122 ◽  
Author(s):  
Hongwei Qin ◽  
Cynthia A. Wilson ◽  
Sun Jung Lee ◽  
Xueyan Zhao ◽  
Etty N. Benveniste
Keyword(s):  
Gene Expression ◽  
Rna Polymerase Ii ◽  
Transcriptional Activation ◽  
Transcriptional Level ◽  
Dependent Manner ◽  
Aberrant Expression ◽  
Endogenous Production ◽  
Cd40 Gene ◽  
Cd40 Expression

AbstractCD40 is expressed on various immune cells, including macrophages and microglia. Aberrant expression of CD40 is associated with autoimmune inflammatory diseases such as multiple sclerosis and rheumatoid arthritis. Interaction of Toll-like receptor-4 (TLR4) with the Gram-negative bacteria endotoxin lipopolysaccharide (LPS) results in the induction of an array of immune response genes. In this study, we describe that LPS is a strong inducer of CD40 expression in macrophages and microglia, which occurs at the transcriptional level and involves the activation of the transcription factors nuclear factor-κB (NF-κB) and signal transducer and activator of transcription 1α (STAT-1α). LPS-induced CD40 expression involves the endogenous production of the cytokine interferon-beta (IFN-β), which contributes to CD40 expression by the activation of STAT-1α. Blocking IFN-β–induced activation of STAT-1α by IFN-β–neutralizing antibody reduces LPS-induced CD40 gene expression. Furthermore, LPS induces acetylation and phosphorylation of histones H3 and H4 and the recruitment of NF-κB, STAT-1α, and RNA polymerase II on the CD40 promoter in vivo in a time-dependent manner, all events important for CD40 gene transcription. These results indicate that both LPS-induced NF-κB activation and endogenous production of IFN-β that subsequently induces STAT-1α activation play critical roles in the transcriptional activation of the CD40 gene by LPS.

scholarly journals Regulation of fibronectin by thyroid hormone receptors

2004 ◽  
Vol 33 (2) ◽  
pp. 445-458 ◽  
Author(s):  
Kwang-Huei Lin ◽  
Chia-yu Chen ◽  
Shen-Liang Chen ◽  
Chun-Che Yen ◽  
Ya-Hui Huang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Thyroid Hormone ◽  
Hormone Receptors ◽  
Transforming Growth Factor ◽  
Thyroid Hormone Receptors ◽  
Transcriptional Level ◽  
Dependent Manner ◽  
Promoter Assay ◽  
Dose Dependent ◽  
P38 Pathway

Thyroid hormones regulate growth, development, differentiation, and metabolic processes by interacting with and activating thyroid hormone receptors and associated pathways. We investigated the triiodothyronine (T3) modulation of gene expression, in human hepatocellular carcinoma cell lines, via a PCR-based cDNA subtraction method. Here we present further data on one of the T3-upregulated genes, fibronectin (FN). We demonstrate that the induction of FN protein expression by T3 in TRα1 and TRβ1 over-expressing cells was time and dose-dependent at the mRNA and protein levels. Blockade of protein synthesis by cycloheximide almost completely inhibited the concomitant induction of FN mRNA by T3, indicating that T3 indirectly regulates FN. Furthermore, nuclear-run on and FN promoter assay clearly can specifically increase the number of FN transcriptional demonstrated that the presence of T3 initiations. In addition, we further confirmed that the up-regulation of FN by T3 was mediated, at least in part, by transforming growth factor-β (TGF-β), because the induction of FN was blocked in a dose-dependent manner by the addition of TGF-β neutralizing antibody. In an effort to elucidate the we demonstrated the involvement of the signaling pathways involved in the activation of FN by T3, mitogen activated protein kinase/c-Jun N-terminal kinase/p38 MAPK (MAPK/JNK/p38) pathway. Although T3 induces the expression of TGF-β, neither wild-type nor dominant-negative Smad3 or Smad4 over-expression affected the activation of FN by T3. Thus, we demonstrate that T3 regulates FN gene expression indirectly at the transcriptional level, with the participation of the MAPK/JNK/p38 pathway and the TGF-β signaling pathway but independent of Smad3/4.

Mechanism of dexamethasone-mediated interleukin-8 gene suppression in cultured airway epithelial cells

2001 ◽  
Vol 280 (1) ◽  
pp. L107-L115 ◽  
Author(s):  
Mary Mann-Jong Chang ◽  
Maya Juarez ◽  
Dallas M. Hyde ◽  
Reen Wu
Keyword(s):  
Gene Expression ◽  
Protein Synthesis ◽  
Epithelial Cells ◽  
Actinomycin D ◽  
Airway Epithelial Cells ◽  
Interleukin 8 ◽  
Transcriptional Level ◽  
Dependent Manner ◽  
Airway Epithelial ◽  
New Protein

The effects of dexamethasone, a glucocorticoid analog, on interleukin 8 (IL-8) gene expression were studied in cultures of primary human tracheobronchial epithelial cells and an immortalized human bronchial epithelial cell line, HBE1 cells. Dexamethasone inhibited IL-8 mRNA and protein expression in a concentration- and time-dependent manner. The inhibition did not occur at the transcriptional level since both nuclear run-on activity and IL-8 promoter-reporter gene expression assay revealed no significant effect. Instead, there was a change in IL-8 mRNA stability in dexamethasone-treated cultures. Under actinomycin D treatment, IL-8 mRNA was quite stable in dexamethasone-depleted cultures, while in dexamethasone-pretreated cultures, IL-8 message was rapidly degraded within the first hour, then leveled off. When dexamethasone and actinomycin D were added simultaneously to dexamethasone-depleted cultures, IL-8 mRNA remained rather stable. When cycloheximide was used to inhibit new protein synthesis, dexamethasone-dependent inhibition was not observed. These results suggest that a posttranscriptional mechanism, which requires dexamethasone-dependent new protein synthesis, is involved in the regulation of IL-8 mRNA by dexamethasone in airway epithelial cells.

scholarly journals Reduced Glutamine Synthetase Activity Alters the Fecundity of Female Bactrocera dorsalis (Hendel)

Insects ◽  
2019 ◽  
Vol 10 (7) ◽  
pp. 186 ◽  
Author(s):  
Dong Wei ◽  
Meng-Yi Zhang ◽  
Ying-Xin Zhang ◽  
Su-Yun Zhang ◽  
Guy Smagghe ◽  
...  
Keyword(s):  
Gene Expression ◽  
Enzyme Activity ◽  
Glutamine Synthetase ◽  
Egg Production ◽  
Fat Body ◽  
Specific Inhibitor ◽  
Bactrocera Dorsalis ◽  
Transcriptional Level ◽  
Synthetase Activity ◽  
Glutamine Synthetase Activity

Glutamine synthetase (GS) is a key enzyme in glutamine synthesis and is associated with multiple physiological processes in insects, such as embryonic development, heat shock response, and fecundity regulation. However, little is known about the influence of GS on female fecundity in the oriental fruit fly, Bactrocera dorsalis. Based on the cloning of BdGSs, mitochondrial BdGSm and cytoplasmic BdGSc, we determined their expressions in the tissues of adult B. dorsalis. BdGSm was highly expressed in the fat body, while BdGSc was highly expressed in the head and midgut. Gene silencing by RNA interference against two BdGSs isoforms suppressed target gene expression at the transcriptional level, leading to a reduced ovarian size and lower egg production. The specific inhibitor L-methionine S-sulfoximine suppressed enzyme activity, but only the gene expression of BdGSm was suppressed. A similar phenotype of delayed ovarian development occurred in the inhibitor bioassay. Significantly lower expression of vitellogenin and vitellogenin receptor was observed when GS enzyme activity was suppressed. These data illustrate the effects of two GS genes on adult fecundity by regulating vitellogenin synthesis in different ways.

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