scholarly journals Molecular Mechanism of a Photoregulated bZIP Transcription Factor and Its Application as a Molecular Tool

2014 ◽  
Vol 54 (6) ◽  
pp. 307-310
Author(s):  
Osamu HISATOMI
Keyword(s):  
Transcription Factor ◽  
Molecular Mechanism ◽  
Bzip Transcription Factor ◽  
Molecular Tool

scholarly journals A combinatorial action of GmMYB176 and GmbZIP5 controls isoflavonoid biosynthesis in soybean (Glycine max)

2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Arun Kumaran Anguraj Vadivel ◽  
Tim McDowell ◽  
Justin B. Renaud ◽  
Sangeeta Dhaubhadel
Keyword(s):  
Transcription Factor ◽  
Hairy Roots ◽  
Defense Mechanisms ◽  
Biosynthetic Pathway ◽  
Bzip Transcription Factor ◽  
Myb Transcription Factor ◽  
In Planta ◽  
Rnai Silencing ◽  
Protein Protein Interaction ◽  
Soybean Roots

AbstractGmMYB176 is an R1 MYB transcription factor that regulates multiple genes in the isoflavonoid biosynthetic pathway, thereby affecting their levels in soybean roots. While GmMYB176 is important for isoflavonoid synthesis, it is not sufficient for the function and requires additional cofactor(s). The aim of this study was to identify the GmMYB176 interactome for the regulation of isoflavonoid biosynthesis in soybean. Here, we demonstrate that a bZIP transcription factor GmbZIP5 co-immunoprecipitates with GmMYB176 and shows protein–protein interaction in planta. RNAi silencing of GmbZIP5 reduced the isoflavonoid level in soybean hairy roots. Furthermore, co-overexpression of GmMYB176 and GmbZIP5 enhanced the level of multiple isoflavonoid phytoallexins including glyceollin, isowighteone and a unique O-methylhydroxy isoflavone in soybean hairy roots. These findings could be utilized to develop biotechnological strategies to manipulate the metabolite levels either to enhance plant defense mechanisms or for human health benefits in soybean or other economically important crops.

Interaction between optineurin and the bZIP transcription factor NRL

2013 ◽  
Vol 38 (1) ◽  
pp. 16-25 ◽  
Author(s):  
Chunxia Wang ◽  
Katsuhiro Hosono ◽  
Masafumi Ohtsubo ◽  
Kentaro Ohishi ◽  
Jie Gao ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Bzip Transcription Factor

scholarly journals Alveolar capillary dysplasia with misalignment of the pulmonary veins: clinical, histological, and genetic aspects

2018 ◽  
Vol 8 (3) ◽  
pp. 204589401879514 ◽  
Author(s):  
Evelien Slot ◽  
Gabriëla Edel ◽  
Ernest Cutz ◽  
Arno van Heijst ◽  
Martin Post ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Molecular Mechanism ◽  
Pulmonary Veins ◽  
Clinical Aspects ◽  
Lung Disorder ◽  
Genetic Studies ◽  
Ongoing Research ◽  
Alveolar Capillary Dysplasia ◽  
Alveolar Capillary ◽  
Severe Lung

Alveolar capillary dysplasia with misalignment of the pulmonary veins (ACD/MPV) is a rare and lethal disorder mainly involving the vascular development of the lungs. Since its first description, significant achievements in research have led to a better understanding of the underlying molecular mechanism of ACD/MPV and genetic studies have identified associations with genomic alterations in the locus of the transcription factor FOXF1. This in turn has increased the awareness among clinicians resulting in over 200 cases reported so far, including genotyping of patients in most recent reports. Collectively, this promoted a better stratification of the patient group, leading to new perspectives in research on the pathogenesis. Here, we provide an overview of the clinical aspects of ACD/MPV, including guidance for clinicians, and review the ongoing research into the complex molecular mechanism causing this severe lung disorder.

Altered expression of the bZIP transcription factor DRINK ME affects growth and reproductive development inArabidopsis thaliana

2016 ◽  
Vol 88 (3) ◽  
pp. 437-451 ◽  
Author(s):  
Paulina Lozano-Sotomayor ◽  
Ricardo A. Chávez Montes ◽  
Marina Silvestre-Vañó ◽  
Humberto Herrera-Ubaldo ◽  
Raffaella Greco ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Reproductive Development ◽  
Bzip Transcription Factor ◽  
Altered Expression

scholarly journals Thyrotroph embryonic factor (TEF) is differentially expressed in high-grade serous ovarian cancers.

2020 ◽  
Author(s):  
Shahan Mamoor
Keyword(s):  
Ovarian Cancer ◽  
Transcription Factor ◽  
Differential Expression ◽  
Expression Profiles ◽  
Gynecologic Cancer ◽  
Bzip Transcription Factor ◽  
High Grade ◽  
Significant Differential Expression ◽  
Primary Tumors ◽  
Embryonic Factor

Ovarian cancer is the most lethal gynecologic cancer (1). We sought to identify genes associated with high-grade serous ovarian cancer (HGSC) by comparing global gene expression profiles of normal ovary with that of primary tumors from women diagnosed with HGSC using published microarray data (2, 3). We previously reported differential expression of the PAR-bZIP transcription factor HLF in HGSC (4). Here, we report significant differential expression of a second PAR-bZIP transcription factor, thyrotroph embryonic factor (TEF) (5) in high-grade serous ovarian tumors.

scholarly journals Transcription Factor ADS-4 Regulates Adaptive Responses and Resistance to Antifungal Azole Stress

2015 ◽  
Vol 59 (9) ◽  
pp. 5396-5404 ◽  
Author(s):  
Kangji Wang ◽  
Zhenying Zhang ◽  
Xi Chen ◽  
Xianyun Sun ◽  
Cheng Jin ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Efflux Pump ◽  
Fungal Infections ◽  
Antifungal Drugs ◽  
Bzip Transcription Factor ◽  
Azole Resistance ◽  
Homologous Gene ◽  
Adaptive Responses ◽  
Transcriptional Responses ◽  
Content Type

ABSTRACTAzoles are commonly used as antifungal drugs or pesticides to control fungal infections in medicine and agriculture. Fungi adapt to azole stress by rapidly activating the transcription of a number of genes, and transcriptional increases in some azole-responsive genes can elevate azole resistance. The regulatory mechanisms that control transcriptional responses to azole stress in filamentous fungi are not well understood. This study identified a bZIP transcription factor, ADS-4 (antifungaldrugsensitive-4), as a new regulator of adaptive responses and resistance to antifungal azoles. Transcription ofads-4inNeurospora crassacells increased when they were subjected to ketoconazole treatment, whereas the deletion ofads-4resulted in hypersensitivity to ketoconazole and fluconazole. In contrast, the overexpression ofads-4increased resistance to fluconazole and ketoconazole inN. crassa. Transcriptome sequencing (RNA-seq) analysis, followed by quantitative reverse transcription (qRT)-PCR confirmation, showed that ADS-4 positively regulated the transcriptional responses of at least six genes to ketoconazole stress inN. crassa. The gene products of four ADS-4-regulated genes are known contributors to azole resistance, including the major efflux pump CDR4 (Pdr5p ortholog), an ABC multidrug transporter (NcAbcB), sterol C-22 desaturase (ERG5), and a lipid transporter (NcRTA2) that is involved in calcineurin-mediated azole resistance. Deletion of theads-4-homologous gene Afads-4inAspergillus fumigatuscaused hypersensitivity to itraconazole and ketoconazole, which suggested that ADS-4 is a functionally conserved regulator of adaptive responses to azoles. This study provides important information on a new azole resistance factor that could be targeted by a new range of antifungal pesticides and drugs.

Pronounced sequence specificity of the TET enzyme catalytic domain guides its cellular function

2021 ◽  
Author(s):  
Mirunalini Ravichandran ◽  
Dominik Rafalski ◽  
Oscar Ortega-Recalde ◽  
Claudia I Davies ◽  
Cassandra R Glanfield ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Binding Sites ◽  
Catalytic Domain ◽  
Transcription Factor Binding Sites ◽  
Transcription Factor Binding ◽  
Dna Demethylation ◽  
Bzip Transcription Factor ◽  
Sequence Specificity ◽  
Transcriptional Responses ◽  
Factor Binding

TET (ten-eleven translocation) enzymes catalyze the oxidation of 5-methylcytosine bases in DNA, thus driving active and passive DNA demethylation. Here, we report that the catalytic cores of mammalian TET enzymes favor CpGs embedded within bHLH and bZIP transcription factor binding sites, with 250-fold preference in vitro. Crystal structures and molecular dynamics calculations show that sequence preference is caused by intra-substrate interactions and CpG flanking sequence indirectly affecting enzyme conformation. TET sequence preferences are physiologically relevant as they explain the rates of DNA demethylation in TET-rescue experiments in culture and in vivo within the zygote and germline. Most and least favorable TET motifs represent DNA sites that are bound by methylation-sensitive immediate-early transcription factors and OCT4, respectively, illuminating TET function in transcriptional responses and pluripotency support. One-Sentence Summary: The catalytic domains of the enzymes that facilitate passive and drive active DNA demethylation have intrinsic sequence preferences that target DNA demethylation to bHLH and bZIP transcription factor binding sites.

Abstract 1384: Osteogenic Transcription Factor Runx2 Regulates Expression of RANKL during VSMC Calcification

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Chang Hyun Byon ◽  
Jay McDonald ◽  
Yabing Chen
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Molecular Mechanism ◽  
Luciferase Reporter ◽  
Rankl Expression ◽  
Reporter System ◽  
Mobility Shift ◽  
Atherosclerotic Lesions ◽  
Flanking Region

The expression of receptor activator of nuclear factor κ B (RANKL) is up-regulated in calcified atherosclerotic lesions, whereas it is frequently undetectable in normal vessels. The underlying molecular mechanism of increased expression of RANKL in calcified vessels is not known. We have previously demonstrated that oxidative stress induces calcification of vascular smooth muscle cells (VSMC) in vitro . Therefore, we determined whether oxidative stress regulates RANKL expression in VSMC and the underlying molecular mechanism. Consistent with previous observations in vivo , we found that the expression of RANKL in VSMC isolated from mouse. However, hydrogen peroxide (H 2 O 2 ), which induces VSMC calcification, induced a 33-fold increase in the transcripts of RANKL as determined by real-time PCR. Increased expression of RANKL protein was further confirmed by ELISA. Using flow cytometry, we demonstrated that membrane-bound RANKL was increased by oxidative stress. To characterize the molecular mechanism underlying H 2 O 2 -induced RANKL expression, we employed the luciferase reporter system with a series of deletion mutants of the RANKL 5′-flanking region. The H 2 O 2 responsive region is located between −200 to −400 in the 5′-flanking region of RANKL gene. Analyses of the sequence of this region identified multiple binding sites for the key osteogenic transcription factor, Runx2, which we previously reported to be an essential regulator of VSMC calcification. Electrophoretic mobility shift analyses demonstrated increased binding of Runx2 on the RANKL promoter sequence in nuclear extracts from VSMC exposed to H 2 O 2 . To further determine the role of Runx2 in regulating RANKL expression, we generated stable Runx2 knockdown VSMC with the use of lentivirus-carrying shRNA for Runx2 gene. H 2 O 2 -induced RANKL expression was abrogated in VSMC with Runx2 knockdown. In addition, adenovirus-mediated overexpression of Runx2 in VSMC induced the expression of RANKL. In summary, we have demonstrated that H 2 O 2 induces the expression of RANKL in VSMC, which is regulated by the osteogenic transcription factor Runx2. These observations provide novel molecular insights into the regulation of RANKL and its role on the pathogenesis of calcified atherosclerotic lesions.

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