scholarly journals Proline as a probable biomarker of cold stress tolerance in Sorghum (Sorghum bicolor)

2018 ◽  
Vol 3 (3) ◽  
pp. 77-86 ◽  
Author(s):  
Pedro Vera-Hernández ◽  
Marco Antonio Ortega-Ramírez ◽  
Marcelino Martínez Nuñez ◽  
Magali Ruiz-Rivas ◽  
Flor de Fátima Rosas-Cárdenas
Keyword(s):  
Cold Stress ◽  
Binding Sites ◽  
Molecular Mechanisms ◽  
Stress Conditions ◽  
Stress Factors ◽  
Free Proline ◽  
Proline Biosynthesis ◽  
Promoter Regions ◽  
Responsive Element ◽  
P5cs Gene

Plants have developed physiological and molecular mechanisms to support and adapt to adverse environments. One response to abiotic stress is the accumulation of free proline (PRO). PRO can induce the expression of many genes, which have the proline-responsive element (PRE) in their promoters, nevertheless due to the complexity of interactions between stress factors and various molecular, biochemical and physiological phenomena it is still unclear whether a more efficient PRO accumulation can be considered a biomarker of tolerance in plants. In the present work, we evaluated the accumulation of PRO in two genotypes of sorghum with contrasting tolerance to cold stress. To explore the cause behind the accumulation of proline under cold stress conditions, we identified the Transcription Factors Binding Sites (TFBS) present in the promoter regions in the genes involved in the biosynthesis and degradation of proline in sorghum and other important crops, finding that the untranslated 3 'region P5CS gene contains different TFBS. We found TFBS that could allow the activation of genes involved in proline biosynthesis through the ornithine pathway under cold stress conditions, suggesting that ornithine route can be activated under cold stress conditions

scholarly journals The tert-butylhydroquinone-mediated activation of the human thioredoxin gene reveals a novel promoter structure

2006 ◽  
Vol 398 (2) ◽  
pp. 269-277 ◽  
Author(s):  
Simone A. Osborne ◽  
Hye-Jin Kim Hawkes ◽  
Ben L. Baldwin ◽  
Kylie A. Alexander ◽  
Terje Svingen ◽  
...  
Keyword(s):  
Binding Sites ◽  
Core Promoter ◽  
Cell Signalling ◽  
Cancer Cell Line ◽  
Regulatory Elements ◽  
Tata Box ◽  
Pcr Analysis ◽  
Promoter Regions ◽  
Thioredoxin System ◽  
Responsive Element

Thioredoxin is a redox-active protein that plays multiple roles in regulating cell growth, cell signalling and apoptosis. Here, we have demonstrated that a complex mechanism involving multiple regulatory elements is involved in the tBHQ [tert-butylhydroquinone or 2,5-di-(t-butyl)-1,4-hydroquinone]-mediated activation of the thioredoxin gene. Luciferase assays, utilizing various wild-type and mutated thioredoxin promoter fragments, revealed roles for the ORE (oxidative stress responsive element), ARE (antioxidant responsive element), three Sp1 (specificity protein 1)-binding sites and the TATA box in the activation of the thioredoxin gene by tBHQ. The ORE required the presence of the ARE to elicit its response, whereas the independent removal of three Sp1-binding sites and the TATA box also decreased activation of the thioredoxin gene, with mutation of the TATA box having the greatest effect. Real-time RT (reverse transcriptase)–PCR analysis also revealed varying roles for two TSSs (transcription start sites) in the activation of the thioredoxin gene by tBHQ. Transcription was initiated from both TSSs; however, different response rates and fold inductions were observed. Together, these results suggest that the thioredoxin gene is controlled by a novel arrangement of two overlapping core promoter regions, one containing a TATA box and the other TATA-less. Altering the intracellular levels of thioredoxin in a breast cancer cell line also influenced the induction of thioredoxin transcription in response to tBHQ. Stable transfections with a redox-inactive thioredoxin mutant produced 3.6 times higher induction levels of thioredoxin transcription compared with control cells, indicating an intrinsic form of control of promoter activity by the thioredoxin system itself.

scholarly journals The Influence of Abiotic Stress Factors on the Morphophysiological and Phytochemical Aspects of the Acclimation of the Plant Rhodiola semenowii Boriss

Plants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1196
Author(s):  
Nina V. Terletskaya ◽  
Nazym K. Korbozova ◽  
Nataliya O. Kudrina ◽  
Tatyana N. Kobylina ◽  
Meruert S. Kurmanbayeva ◽  
...  
Keyword(s):  
Photosystem Ii ◽  
Cold Stress ◽  
Water Deficit ◽  
Cold Treatment ◽  
Photosynthetic Apparatus ◽  
Stress Conditions ◽  
Stress Factors ◽  
Gas Chromatography Mass Spectrometry ◽  
Quantitative Composition ◽  
Plant Tissues

Plants of the Crassulaceae family are natural accumulators of many medicinal secondary metabolites (SM). This article describes the study of morphophysiological, anatomic and phytochemical responses of immature plants of Rhodiolla semenovii under water deficit and (or) cold-stress conditions. Changes in biomass production due to water content in plant tissues such as a decrease in water deficit and an increase in cold stress were revealed. A significant decrease in the efficiency of the photosynthetic apparatus under stress conditions was noted, based on the parameters quantum efficiency of Photosystem II and electron transport rate and energy dissipated in Photosystem II. The greatest decrease in efficiency was pointed out in conditions of water shortage. The anatomical modulations of root and shoot of R. semenovii under stress conditions were found. For the first time, a detailed study of the chemical composition of the ethanol extract of root and shoot of R. semenovii under stress was carried out using gas chromatography–mass spectrometry. The qualitative and quantitative composition of SM associated with acclimation to the effects of abiotic stresses was determined. Both nonspecific and specific phytochemical changes caused by the action of water deficiency and cold treatment were identified. It has been shown that the antioxidant system in plant tissues is complex, multicomponent, depending on a number of natural and climatic factors. Further research should be focused on the use of abiotic stressors for the targeted synthesis of bioactive SMs valuable for pharmaceutical use.

scholarly journals C/EBPδ-induced epigenetic changes control the dynamic gene transcription of S100A8 and S100A9

2021 ◽  
Author(s):  
Saskia-Larissa Jauch-Speer ◽  
Jonas Wolf ◽  
Marisol Herrera-Rivero ◽  
Leonie Martens ◽  
Achmet Imam Chasan ◽  
...  
Keyword(s):  
Binding Sites ◽  
Molecular Mechanisms ◽  
Epigenetic Changes ◽  
Promoter Regions ◽  
Inflammatory Conditions ◽  
Genome Wide ◽  
Promising Target ◽  
Cardiovascular Patients ◽  
Factor C ◽  
S100a9 Expression

The proinflammatory alarmins S100A8 and S100A9 are among the most abundant proteins in neutrophils and monocytes but completely silenced after differentiation to macrophages. The molecular mechanisms of the extraordinarily dynamic transcriptional regulation of s100a8 and s100a9 genes, however, are only barely understood. Using an unbiased genome-wide CRISPR/Cas9 knockout based screening approach in immortalized murine monocytes we identified the transcription factor C/EBPδ as a central regulator of S100A8 and S100A9 expression. S100a8 and S100a9 expression was further controlled by the C/EBPδ-antagonists ATF3 and FBXW7. We confirmed the clinical relevance of this regulatory network in subpopulations of human monocytes in a clinical cohort of cardiovascular patients. Moreover, we identified specific C/EBPδ-binding sites within s100a8 and s100a9 promoter regions, and demonstrated that C/EBPδ-dependent JMJD3-mediated demethylation of H3K27me3 is indispensable for their expression. Overall, our work uncovered C/EBPδ as a novel regulator of S100A8 and S100A9 expression. Therefore, C/EBPδ represents a promising target for modulation of inflammatory conditions that are characterised by S100A8 and S100A9 overexpression.

scholarly journals Analysis of Haloferax mediterranei Lrp Transcriptional Regulator

Genes ◽  
2021 ◽  
Vol 12 (6) ◽  
pp. 802
Author(s):  
Laura Matarredona ◽  
Mónica Camacho ◽  
María-José García-Bonete ◽  
Belén Esquerra ◽  
Basilio Zafrilla ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Gene Expression Regulation ◽  
Gel Filtration ◽  
Transcriptional Regulator ◽  
Nitrogen Sources ◽  
Transcriptional Factor ◽  
Stress Conditions ◽  
Stress Factors ◽  
Haloferax Mediterranei ◽  
General Response

Haloferax mediterranei is an extremely halophilic archaeon, able to live in hypersaline environments with versatile nutritional requirements, whose study represents an excellent basis in the field of biotechnology. The transcriptional machinery in Archaea combines the eukaryotic basal apparatus and the bacterial regulation mechanisms. However, little is known about molecular mechanisms of gene expression regulation compared with Bacteria, particularly in Haloarchaea. The genome of Hfx. mediterranei contains a gene, lrp (HFX_RS01210), which encodes a transcriptional factor belonging to Lrp/AsnC family. It is located downstream of the glutamine synthetase gene (HFX_RS01205), an enzyme involved in ammonium assimilation and amino acid metabolism. To study this transcriptional factor more deeply, the lrp gene has been homologously overexpressed and purified under native conditions by two chromatographic steps, namely nickel affinity and gel filtration chromatography, showing that Lrp behaves asa tetrameric protein of approximately 67 kDa. Its promoter region has been characterized under different growth conditions using bgaH as a reporter gene. The amount of Lrp protein was also analyzed by Western blotting in different nitrogen sources and under various stress conditions. To sum up, regarding its involvement in the nitrogen cycle, it has been shown that its expression profile does not change in response to the nitrogen sources tested. Differences in its expression pattern have been observed under different stress conditions, such as in the presence of hydrogen peroxide or heavy metals. According to these results, the Lrp seems to be involved in a general response against stress factors, acting as a first-line transcriptional regulator.

Strategies to Protect Hematopoietic Stem Cells from Culture-Induced Stress Conditions

2020 ◽  
Vol 15 ◽  
Author(s):  
Fatima Aerts-Kaya
Keyword(s):  
Stem Cells ◽  
Hematopoietic Stem Cells ◽  
Ex Vivo ◽  
Stress Conditions ◽  
Stress Factors ◽  
Hematopoietic Stem ◽  
Induced Stress

: In contrast to their almost unlimited potential for expansion in vivo and despite years of dedicated research and optimization of expansion protocols, the expansion of Hematopoietic Stem Cells (HSCs) in vitro remains remarkably limited. Increased understanding of the mechanisms that are involved in maintenance, expansion and differentiation of HSCs will enable the development of better protocols for expansion of HSCs. This will allow procurement of HSCs with long-term engraftment potential and a better understanding of the effects of the external influences in and on the hematopoietic niche that may affect HSC function. During collection and culture of HSCs, the cells are exposed to suboptimal conditions that may induce different levels of stress and ultimately affect their self-renewal, differentiation and long-term engraftment potential. Some of these stress factors include normoxia, oxidative stress, extra-physiologic oxygen shock/stress (EPHOSS), endoplasmic reticulum (ER) stress, replicative stress, and stress related to DNA damage. Coping with these stress factors may help reduce the negative effects of cell culture on HSC potential, provide a better understanding of the true impact of certain treatments in the absence of confounding stress factors. This may facilitate the development of better ex vivo expansion protocols of HSCs with long-term engraftment potential without induction of stem cell exhaustion by cellular senescence or loss of cell viability. This review summarizes some of available strategies that may be used to protect HSCs from culture-induced stress conditions.

scholarly journals Genes encoding components of the olfactory signal transduction cascade contain a DNA binding site that may direct neuronal expression.

1993 ◽  
Vol 13 (9) ◽  
pp. 5805-5813 ◽  
Author(s):  
M M Wang ◽  
R Y Tsai ◽  
K A Schrader ◽  
R R Reed
Keyword(s):  
Signal Transduction ◽  
Dna Binding ◽  
Binding Site ◽  
Binding Sites ◽  
Consensus Sequence ◽  
Initiation Site ◽  
Olfactory Neuron ◽  
Promoter Regions ◽  
Transcriptional Initiation ◽  
Genes Encoding

Genes which mediate odorant signal transduction are expressed at high levels in neurons of the olfactory epithelium. The molecular mechanism governing the restricted expression of these genes likely involves tissue-specific DNA binding proteins which coordinately activate transcription through sequence-specific interactions with olfactory promoter regions. We have identified binding sites for the olfactory neuron-specific transcription factor, Olf-1, in the sequences surrounding the transcriptional initiation site of five olfactory neuron-specific genes. The Olf-1 binding sites described define the consensus sequence YTCCCYRGGGAR. In addition, we have identified a second binding site, the U site, in the olfactory cyclic nucleotide gated channel and type III cyclase promoters, which binds factors present in all tissue examined. These experiments support a model in which expression of Olf-1 in the sensory neurons coordinately activates a set of olfactory neuron-specific genes. Furthermore, expression of a subset of these genes may be modulated by additional binding factors.

scholarly journals Induction of the Cellular E2F-1 Promoter by the Adenovirus E4-6/7 Protein

2000 ◽  
Vol 74 (5) ◽  
pp. 2084-2093 ◽  
Author(s):  
Joel Schaley ◽  
Robert J. O'Connor ◽  
Laura J. Taylor ◽  
Dafna Bar-Sagi ◽  
Patrick Hearing
Keyword(s):  
Dna Binding ◽  
Binding Site ◽  
Transient Expression ◽  
Binding Sites ◽  
Promoter Region ◽  
Fluorescent Protein ◽  
Protein Accumulation ◽  
Promoter Regions ◽  
Single Binding Site

ABSTRACT The adenovirus type 5 (Ad5) E4-6/7 protein interacts directly with different members of the E2F family and mediates the cooperative and stable binding of E2F to a unique pair of binding sites in the Ad5 E2a promoter region. This induction of E2F DNA binding activity strongly correlates with increased E2a transcription when analyzed using virus infection and transient expression assays. Here we show that while different adenovirus isolates express an E4-6/7 protein that is capable of induction of E2F dimerization and stable DNA binding to the Ad5 E2a promoter region, not all of these viruses carry the inverted E2F binding site targets in their E2a promoter regions. The Ad12 and Ad40 E2a promoter regions bind E2F via a single binding site. However, these promoters bind adenovirus-induced (dimerized) E2F very weakly. The Ad3 E2a promoter region binds E2F very poorly, even via a single binding site. A possible explanation of these results is that the Ad E4-6/7 protein evolved to induce cellular gene expression. Consistent with this notion, we show that infection with different adenovirus isolates induces the binding of E2F to an inverted configuration of binding sites present in the cellular E2F-1 promoter. Transient expression of the E4-6/7 protein alone in uninfected cells is sufficient to induce transactivation of the E2F-1 promoter linked to chloramphenicol acetyltransferase or green fluorescent protein reporter genes. Further, expression of the E4-6/7 protein in the context of adenovirus infection induces E2F-1 protein accumulation. Thus, the induction of E2F binding to the E2F-1 promoter by the E4-6/7 protein observed in vitro correlates with transactivation of E2F-1 promoter activity in vivo. These results suggest that adenovirus has evolved two distinct mechanisms to induce the expression of the E2F-1 gene. The E1A proteins displace repressors of E2F activity (the Rb family members) and thus relieve E2F-1 promoter repression; the E4-6/7 protein complements this function by stably recruiting active E2F to the E2F-1 promoter to transactivate expression.

scholarly journals Enhancing the Nrf2 Antioxidant Signaling Provides Protection Against Trichloroethene-mediated Inflammation and Autoimmune Response

2020 ◽  
Vol 175 (1) ◽  
pp. 64-74 ◽  
Author(s):  
Nivedita Banerjee ◽  
Hui Wang ◽  
Gangduo Wang ◽  
M Firoze Khan
Keyword(s):  
Oxidative Stress ◽  
T Cells ◽  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Autoimmune Response ◽  
Mediated Effects ◽  
Antioxidant Gene Expression ◽  
Responsive Element

Abstract Trichloroethene (trichloroethylene, TCE) and one of its reactive metabolites dichloroacetyl chloride (DCAC) are associated with the induction of autoimmunity in MRL+/+ mice. Although oxidative stress plays a major role in TCE-/DCAC-mediated autoimmunity, the underlying molecular mechanisms still need to be delineated. Nuclear factor (erythroid-derived 2)-like2 (Nrf2) is an oxidative stress-responsive transcription factor that binds to antioxidant responsive element (ARE) and provides protection by regulating cytoprotective and antioxidant gene expression. However, the potential of Nrf2 in the regulation of TCE-/DCAC-mediated autoimmunity is not known. This study thus focused on establishing the role of Nrf2 and consequent inflammatory responses in TCE-/DCAC-mediated autoimmunity. To achieve this, we pretreated Kupffer cells (KCs) or T cells with/without tert-butylhydroquinone (tBHQ) followed by treatment with DCAC. In both KCs and T cells, DCAC treatment significantly downregulated Nrf2 and HO-1 expression along with induction of Keap-1 and caspase-3, NF-κB (p65), TNF-α, and iNOS, whereas pretreatment of these cells with tBHQ attenuated these responses. The in vitro findings were further verified in vivo by treating female MRL+/+ mice with TCE along with/without sulforaphane. TCE exposure in mice also led to reduction in Nrf2 and HO-1 but increased phospho-NF-κB (p-p65) and iNOS along with increased anti-dsDNA antibodies. Interestingly, sulforaphane treatment led to amelioration of TCE-mediated effects, resulting in Nrf2 activation and reduction in inflammatory and autoimmune responses. Our results show that TCE/DCAC mediates an impairment in Nrf2 regulation. Attenuation of TCE-mediated autoimmunity via activation of Nrf2 supports that antioxidants sulforaphane/tBHQ could be potential therapeutic agents for autoimmune diseases.

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