Abiotic-stress induces demethylation and transcriptional activation of a gene encoding a glycerophosphodiesterase-like protein in tobacco plants

2007 ◽  
Vol 277 (5) ◽  
pp. 589-600 ◽  
Author(s):  
Chang-Sun Choi ◽  
Hiroshi Sano
Keyword(s):  
Abiotic Stress ◽  
Transcriptional Activation ◽  
Gene Encoding ◽  
Tobacco Plants

scholarly journals Design of Construct Carrying GmDREB6 to Enhance Soybean Gene Expression Related to Abiotic Stress Response

2019 ◽  
Vol 4 (6) ◽  
pp. 135-139
Author(s):  
Lan Thi Ngoc Nguyen ◽  
Phutthakine Vaciaxa ◽  
Thu Thi Mai Lo ◽  
Yen Thi Hai Nguyen ◽  
Nhan Thi Thanh Pham ◽  
...  
Keyword(s):  
Abiotic Stress ◽  
Stress Factors ◽  
Transcriptional Level ◽  
Abiotic Stress Response ◽  
Gene Encoding ◽  
Tobacco Plants ◽  
Glycine Max L ◽  
Soybean Gene ◽  
Soybean Plants ◽  
Artificial Gene

Glycine max (L.) Merrill is a crop that brings a lot of economic and nutritive values, however soybean is quite sensitive to stress. The applications of gene technology can improve resistance of soybean plants against external stress factors. The aim of this study was to conduct a transgenic vector containing GmDREB6 gene and determine the expression of gene encoding GmDREB6 in Nicotiana tabacum before transforming into soybean plants. The GmDREB6 artificial gene was synthesized containing nucleotide fragment encoding 230 amino acids, nucleotide fragment encoding cmyc antigen and nucleotide fragments with cut-off points of XbaI/SacI enzyme pair. The results indicated that the 35S-GmDREB6-cmyc construct was designed and transferred into tobacco plants. The GmDREB6 was incorporated in the genome and was expressed in transgenic tobacco plants at the transcriptional level. The transgenic vector pBI121_GmDREB6 well worked on the model tobacco plants. Therefore, it can be used for transferring into soybean plants to enhance soybean tolerance to abiotic stress.

The orphan nuclear receptor NGFI-B regulates expression of the gene encoding steroid 21-hydroxylase

1993 ◽  
Vol 13 (2) ◽  
pp. 861-868
Author(s):  
T E Wilson ◽  
A R Mouw ◽  
C A Weaver ◽  
J Milbrandt ◽  
K L Parker
Keyword(s):  
Nuclear Receptor ◽  
Transcriptional Activation ◽  
Core Promoter ◽  
Orphan Nuclear Receptor ◽  
Recognition Sequence ◽  
Mobility Shift ◽  
Adrenocortical Cells ◽  
Gene Encoding ◽  
Adult Rat ◽  
Gel Mobility Shift

As part of its trophic action to maintain the steroidogenic capacity of adrenocortical cells, corticotropin (ACTH) increases the transcription of the cytochrome P-450 steroid hydroxylase genes, including the gene encoding steroid 21-hydroxylase (21-OHase). We previously identified several promoter elements that regulate 21-OHase gene expression in mouse Y1 adrenocortical tumor cells. One of these elements, located at nucleotide -65, closely resembles the recognition sequence of the orphan nuclear receptor NGFI-B, suggesting that NGFI-B regulates this essential steroidogenic enzyme. To explore this possibility, we first used in situ hybridization to demonstrate high levels of NGFI-B transcripts in the adrenal cortex of the adult rat. In cultured mouse Y1 adrenocortical cells, treatment with ACTH, the major regulator of 21-OHase transcription, rapidly increased NGFI-B expression. Gel mobility shift and DNase I footprinting experiments showed that recombinantly expressed NGFI-B interacts specifically with the 21-OHase -65 element and identified one complex formed by Y1 extracts and the 21-OHase -65 element that contains NGFI-B. Expression of NGFI-B significantly augmented the activity of the intact 21-OHase promoter, while mutations of the -65 element that abolish NGFI-B binding markedly diminished NGFI-B-mediated transcriptional activation. Specific mutations of NGFI-B shown previously to impair either DNA binding or transcriptional activation diminished the effect of NGFI-B coexpression on 21-OHase expression. Finally, an oligonucleotide containing the NGFI-B response element conferred ACTH response to a core promoter from the prolactin gene, showing that this element is sufficient for ACTH induction. Collectively, these results identify a cellular promoter element that is regulated by NGFI-B and implicate NGFI-B in the transcriptional induction of 21-OHase by ACTH.

scholarly journals Activation of the Akt1-CREB pathway promotes RNF146 expression to inhibit PARP1-mediated neuronal death

2020 ◽  
Vol 13 (663) ◽  
pp. eaax7119
Author(s):  
Hyojung Kim ◽  
Jisoo Park ◽  
Hojin Kang ◽  
Seung Pil Yun ◽  
Yun-Song Lee ◽  
...  
Keyword(s):  
Chlorogenic Acid ◽  
Transcriptional Activation ◽  
Dopaminergic Neurons ◽  
Cultured Cells ◽  
Intraperitoneal Administration ◽  
Neuronal Loss ◽  
Postmortem Brain ◽  
Dependent Manner ◽  
Gene Encoding ◽  
Creb Pathway

Progressive degeneration of dopaminergic neurons characterizes Parkinson’s disease (PD). This neuronal loss occurs through diverse mechanisms, including a form of programmed cell death dependent on poly(ADP-ribose) polymerase-1 (PARP1) called parthanatos. Deficient activity of the kinase Akt1 and aggregation of the protein α-synuclein are also implicated in disease pathogenesis. Here, we found that Akt1 suppressed parthanatos in dopaminergic neurons through a transcriptional mechanism. Overexpressing constitutively active Akt1 in SH-SY5Y cells or culturing cells with chlorogenic acid (a polyphenol found in coffee that activates Akt1) stimulated the CREB-dependent transcriptional activation of the gene encoding the E3 ubiquitin ligase RNF146. RNF146 inhibited PARP1 not through its E3 ligase function but rather by binding to and sequestering PAR, which enhanced the survival of cultured cells exposed to the dopaminergic neuronal toxin 6-OHDA or α-synuclein aggregation. In mice, intraperitoneal administration of chlorogenic acid activated the Akt1-CREB-RNF146 pathway in the brain and provided neuroprotection against both 6-OHDA and combinatorial α-synucleinopathy in an RNF146-dependent manner. Furthermore, dysregulation of the Akt1-CREB pathway was observed in postmortem brain samples from patients with PD. The findings suggest that therapeutic restoration of RNF146 expression, such as by activating the Akt1-CREB pathway, might halt neurodegeneration in PD.

scholarly journals Adenovirus E1A specifically blocks SWI/SNF-dependent transcriptional activation.

1996 ◽  
Vol 16 (10) ◽  
pp. 5737-5743 ◽  
Author(s):  
M E Miller ◽  
B R Cairns ◽  
R S Levinson ◽  
K R Yamamoto ◽  
D A Engel ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Cellular Transformation ◽  
Transcriptional Coactivator ◽  
Gene Encoding ◽  
Adenovirus E1a ◽  
Transcriptional Regulatory ◽  
Genes Encoding ◽  
Regulatory Complex ◽  
Activation Pathways ◽  
Coactivator P300

Expression of the adenovirus E1A243 oncoprotein in Saccharomyces cerevisiae produces a slow-growth phenotype with accumulation of cells in the G1 phase of the cell cycle. This effect is due to the N-terminal and CR1 domains of E1A243, which in rodent cells are involved in triggering cellular transformation and also in binding to the cellular transcriptional coactivator p300. A genetic screen was undertaken to identify genes required for the function of E1A243 in S. cerevisiae. This screen identified SNF12, a gene encoding the 73-kDa subunit of the SWI/SNF transcriptional regulatory complex. Mutation of genes encoding known members of the SWI/SNF complex also led to loss of E1A function, suggesting that the SWI/SNF complex is a target of E1A243. Moreover, expression of E1A in wild-type cells specifically blocked transcriptional activation of the INO1 and SUC2 genes, whose activation pathways are distinct but have a common requirement for the SWI/SNF complex. These data demonstrate a specific functional interaction between E1A and the SWI/SNF complex and suggest that a similar interaction takes place in rodent and human cells.

scholarly journals Thrombasthenic mice generated by replacement of the integrin αIIb gene: demonstration that transcriptional activation of this megakaryocytic locus precedes lineage commitment

Blood ◽  
2000 ◽  
Vol 96 (4) ◽  
pp. 1399-1408 ◽  
Author(s):  
Diana Tronik-Le Roux ◽  
Valérie Roullot ◽  
Christel Poujol ◽  
Thierry Kortulewski ◽  
Paquita Nurden ◽  
...  
Keyword(s):  
Transcriptional Activation ◽  
Fibrin Clot ◽  
Lineage Commitment ◽  
Gene Encoding ◽  
Α Subunit ◽  
Knock Out ◽  
Toxic Gene ◽  
Specific Locus ◽  
Deficient Mice

Abstract To analyze the transcriptional activity of the gene encoding the α subunit of the platelet integrin αIIbβ3during the hematopoietic differentiation, mice were produced in which the herpes virus thymidine kinase (tk) was introduced in this megakaryocytic specific locus using homologous recombination technology. This provided a convenient manner in which to induce the eradication of particular hematopoietic cells expressing the targeted gene. Results of progenitor cell cultures and long-term bone marrow (BM) assays showed that the growth of a subset of stem cells was reduced in the presence of the antiherpetic drug ganciclovir, demonstrating that the activation of the toxic gene occurs before the commitment to the megakaryocytic lineage. Furthermore theknock-in of the tk gene into the αIIb locus resulted in the knock-out of the αIIb gene in homozygous mice. Cultures of BM cells of these animals, combined with ultrastructural analysis, established that the αIIbglycoprotein is dispensable for lineage commitment and megakaryocytic maturation. Platelets collected from αIIb-deficient mice failed to bind fibrinogen, to aggregate, and to retract a fibrin clot. Moreover, platelet α-granules did not contain fibrinogen. Consistent with these characteristics, the mice displayed bleeding disorders similar to those in humans with Glanzmann thrombasthenia.

Sign in / Sign up

Export Citation Format

Share Document