Archaeal promoter architecture and mechanism of gene activation

2011 ◽  
Vol 39 (1) ◽  
pp. 99-103 ◽  
Author(s):  
Nan Peng ◽  
Xiang Ao ◽  
Yun Xiang Liang ◽  
Qunxin She
Keyword(s):  
Gene Expression ◽  
Regulatory Element ◽  
Gene Activation ◽  
Inducible Expression ◽  
Promoter Architecture ◽  
Sulfolobus Islandicus ◽  
Binding Factor ◽  
Differential Gene ◽  
Archaeal Gene ◽  
Activate Gene

Sulfolobus solfataricus and Sulfolobus islandicus contain several genes exhibiting D-arabinose-inducible expression and these systems are ideal for studying mechanisms of archaeal gene expression. At sequence level, only two highly conserved cis elements are present on the promoters: a regulatory element named ara box directing arabinose-inducible expression and the basal promoter element TATA, serving as the binding site for the TATA-binding protein. Strikingly, these promoters possess a modular structure that allows an essentially inactive basal promoter to be strongly activated. The invoked mechanisms include TFB (transcription factor B) recruitment by the ara-box-binding factor to activate gene expression and modulation of TFB recruitment efficiency to yield differential gene expression.

scholarly journals Identification of a Ty1 regulatory sequence responsive to STE7 and STE12.

1988 ◽  
Vol 8 (6) ◽  
pp. 2545-2554 ◽  
Author(s):  
M Company ◽  
C Adler ◽  
B Errede
Keyword(s):  
Gene Expression ◽  
Complex Formation ◽  
Reporter Gene ◽  
Regulatory Element ◽  
Gene Activation ◽  
Cell Types ◽  
Reporter Gene Expression ◽  
Regulatory Sequence ◽  
Gene Products ◽  
Cell Extracts

Ty1 activation of gene expression observed in haploid cell types of Saccharomyces cerevisiae requires the STE7 and STE12 gene products. An activator sequence within Ty1 that is responsive to these two regulators has been defined. Complex formation between a factor in whole-cell extracts and the DNA regulatory element showed the same dependence on the STE7 and STE12 gene products as did reporter gene expression. Base pair substitutions within the binding site abolished the ability to form the factor-DNA complex and to activate gene expression. The correlation between complex formation and reporter gene expression indicates that factor binding to the cis-acting element is essential for gene activation. Because the predicted protein for the STE7 gene product is homologous to protein kinases, we suggest that protein phosphorylation may directly or indirectly regulate formation of this DNA-protein complex.

scholarly journals Identification and characterization of a silencer regulatory element in the 3′-flanking region of the murine CD46 gene

2000 ◽  
Vol 351 (2) ◽  
pp. 353-365 ◽  
Author(s):  
Midori NOMURA ◽  
Akira TSUJIMURA ◽  
Nasim A. BEGUM ◽  
Misako MATSUMOTO ◽  
Hiroetsu WABIKO ◽  
...  
Keyword(s):  
Gene Expression ◽  
Reporter Gene ◽  
Stop Codon ◽  
Regulatory Element ◽  
Luciferase Reporter ◽  
Size Difference ◽  
Binding Factor ◽  
Gene Assay ◽  
Flanking Region ◽  
Silencer Element

The murine membrane cofactor protein (CD46) gene is expressed exclusively in testis, in contrast to human CD46, which is expressed ubiquitously. To elucidate the mechanism of differential CD46 gene expression among species, we cloned entire murine CD46 genomic DNA and possible regulatory regions were placed in the flanking region of the luciferase reporter gene. The reporter gene assay revealed a silencing activity not in the promoter, but in the 3´-flanking region of the gene and the silencer-like element was identified within a 0.2-kb region between 0.6 and 0.8kb downstream of the stop codon. This silencer-like element was highly similar to that of the pig MHC class-I gene. The introduction of a mutation into this putative silencer element of murine CD46 resulted in an abrogation of the silencing effect. Electrophoretic mobility-shift assay indicated the presence of the binding molecule(s) for this silencer sequence in murine cell lines and tissues. A size difference of the protein–silencer-element complex was observed depending upon the solubilizers used for preparation of the nuclear extracts. A mutated silencer sequence failed to interact with the binding molecules. The level of the binding factor was lower in the testicular germ cells compared with other organs. Thus the silencer element and its binding factor may play a role in transcriptional regulation of murine CD46 gene expression. These results imply that the effects of the CD46 silencer element encompass the innate immune and reproductive systems, and in mice may determine the testicular germ-cell-dominant expression of CD46.

A GATA-dependent nkx-2.5 regulatory element activates early cardiac gene expression in transgenic mice

Development ◽  
1998 ◽  
Vol 125 (22) ◽  
pp. 4461-4470 ◽  
Author(s):  
R.D. Searcy ◽  
E.B. Vincent ◽  
C.M. Liberatore ◽  
K.E. Yutzey
Keyword(s):  
Gene Expression ◽  
Transgenic Mice ◽  
Expression Pattern ◽  
Binding Sites ◽  
Early Stage ◽  
Regulatory Element ◽  
Gene Activation ◽  
Flanking Sequence ◽  
Regulatory Factors ◽  
Developing Heart

nkx-2.5 is one of the first genes expressed in the developing heart of early stage vertebrate embryos. Cardiac expression of nkx-2.5 is maintained throughout development and nkx-2.5 also is expressed in the developing pharyngeal arches, spleen, thyroid and tongue. Genomic sequences flanking the mouse nkx-2.5 gene were analyzed for early developmental regulatory activity in transgenic mice. Approximately 3 kb of 5′ flanking sequence is sufficient to activate gene expression in the cardiac crescent as early as E7.25 and in limited regions of the developing heart at later stages. Expression also was detected in the developing spleen anlage at least 24 hours before the earliest reported spleen marker and in the pharyngeal pouches and their derivatives including the thyroid. The observed expression pattern from the −3 kb construct represents a subset of the endogenous nkx-2.5 expression pattern which is evidence for compartment-specific nkx-2.5 regulatory modules. A 505 bp regulatory element was identified that contains multiple GATA, NKE, bHLH, HMG and HOX consensus binding sites. This element is sufficient for gene activation in the cardiac crescent and in the heart outflow tract, pharynx and spleen when linked directly to lacZ or when positioned adjacent to the hsp68 promoter. Mutation of paired GATA sites within this element eliminates gene activation in the heart, pharynx and spleen primordia of transgenic embryos. The dependence of this nkx-2. 5 regulatory element on GATA sites for gene activity is evidence for a GATA-dependent regulatory mechanism controlling nkx-2.5 gene expression. The presence of consensus binding sites for other developmentally important regulatory factors within the 505 bp distal element suggests that combinatorial interactions between multiple regulatory factors are responsible for the initial activation of nkx-2.5 in the cardiac, thyroid and spleen primordia.

scholarly journals Nuclear Localization and Formation of β-Catenin–Lymphoid Enhancer Factor 1 Complexes Are Not Sufficient for Activation of Gene Expression

1999 ◽  
Vol 19 (6) ◽  
pp. 4503-4515 ◽  
Author(s):  
Mary G. Prieve ◽  
Marian L. Waterman
Keyword(s):  
Gene Expression ◽  
Reporter Gene ◽  
Nuclear Localization ◽  
Gene Activation ◽  
Wnt Signaling Pathway ◽  
T Cell Factor ◽  
Lymphocyte Cell ◽  
Lymphocyte Cell Line ◽  
Activate Gene ◽  
Enhancer Factor

ABSTRACT In response to activation of the Wnt signaling pathway, β-catenin accumulates in the nucleus, where it cooperates with LEF/TCF (for lymphoid enhancer factor and T-cell factor) transcription factors to activate gene expression. The mechanisms by which β-catenin undergoes this shift in location and participates in activation of gene transcription are unknown. We demonstrate here that β-catenin can be imported into the nucleus independently of LEF/TCF binding, and it may also be exported from nuclei. We have introduced a small deletion within β-catenin (Δ19) that disrupts binding to LEF-1, E-cadherin, and APC but not axin. This Δ19 β-catenin mutant localizes to the nucleus because it may not be efficiently sequestered in the cytoplasm. The nuclear localization of Δ19 definitively demonstrates that the mechanisms by which β-catenin localizes in the nucleus are completely independent of LEF/TCF factors. β-Catenin and LEF-1 complexes can activate reporter gene expression in a transformed T-lymphocyte cell line (Jurkat) but not in normal T lymphocytes, even though both factors are nuclear. Thus, localization of both factors to the nucleus is not sufficient for activation of gene expression. Excess β-catenin can squelch reporter gene activation by LEF-1–β-catenin complexes but not activation by the transcription factor VP16. Taken together, these data suggest that a third component is necessary for gene activation and that this third component may vary with cell type.

scholarly journals Investigating crosstalk between H3K27 acetylation and H3K4 trimethylation in CRISPR/dCas-based epigenome editing and gene activation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Weiye Zhao ◽  
Ying Xu ◽  
Yufan Wang ◽  
Dan Gao ◽  
Jasmine King ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transcriptional Activation ◽  
Gene Activation ◽  
Histone H3 ◽  
Activation Process ◽  
Epigenome Editing ◽  
Transcriptional Start Sites ◽  
Expression Status ◽  
Activate Gene ◽  
Active Genes

AbstractEpigenome editing methods enable the precise manipulation of epigenetic modifications, such as histone posttranscriptional modifications (PTMs), for uncovering their biological functions. While histone PTMs have been correlated with certain gene expression status, the causalities remain elusive. Histone H3 Lysine 27 acetylation (H3K27ac) and histone H3 Lysine 4 trimethylation (H3K4me3) are both associated with active genes, and located at active promoters and enhancers or around transcriptional start sites (TSSs). Although crosstalk between histone lysine acetylation and H3K4me3 has been reported, relationships between specific epigenetic marks during transcriptional activation remain largely unclear. Here, using clustered regularly interspaced short palindromic repeats (CRISPR)/dCas-based epigenome editing methods, we discovered that the ectopic introduction of H3K27ac in the promoter region lead to H3K4me3 enrichment around TSS and transcriptional activation, while H3K4me3 installation at the promoter cannot induce H3K27ac increase and failed to activate gene expression. Blocking the reading of H3K27ac by BRD proteins using inhibitor JQ1 abolished H3K27ac-induced H3K4me3 installation and downstream gene activation. Furthermore, we uncovered that BRD2, not BRD4, mediated H3K4me3 installation and gene activation upon H3K27ac writing. Our studies revealed the relationships between H3K27ac and H3K4me3 in gene activation process and demonstrated the application of CRISPR/dCas-based epigenome editing methods in elucidating the crosstalk between epigenetic mechanisms.

scholarly journals Identification of a Ty1 regulatory sequence responsive to STE7 and STE12

1988 ◽  
Vol 8 (6) ◽  
pp. 2545-2554
Author(s):  
M Company ◽  
C Adler ◽  
B Errede
Keyword(s):  
Gene Expression ◽  
Complex Formation ◽  
Reporter Gene ◽  
Regulatory Element ◽  
Gene Activation ◽  
Cell Types ◽  
Reporter Gene Expression ◽  
Regulatory Sequence ◽  
Gene Products ◽  
Cell Extracts

Ty1 activation of gene expression observed in haploid cell types of Saccharomyces cerevisiae requires the STE7 and STE12 gene products. An activator sequence within Ty1 that is responsive to these two regulators has been defined. Complex formation between a factor in whole-cell extracts and the DNA regulatory element showed the same dependence on the STE7 and STE12 gene products as did reporter gene expression. Base pair substitutions within the binding site abolished the ability to form the factor-DNA complex and to activate gene expression. The correlation between complex formation and reporter gene expression indicates that factor binding to the cis-acting element is essential for gene activation. Because the predicted protein for the STE7 gene product is homologous to protein kinases, we suggest that protein phosphorylation may directly or indirectly regulate formation of this DNA-protein complex.

Differential gene activation by glucocorticoids and progestins through the hormone regulatory element of mouse mammary tumor virus

Cell ◽  
1988 ◽  
Vol 53 (3) ◽  
pp. 371-382 ◽  
Author(s):  
Georges Chalepakis ◽  
Jutta Arnemann ◽  
Emily Slater ◽  
Hans-Joachim Brüller ◽  
Bernhard Gross ◽  
...  
Keyword(s):  
Mammary Tumor ◽  
Mouse Mammary Tumor Virus ◽  
Regulatory Element ◽  
Gene Activation ◽  
Mammary Tumor Virus ◽  
Mouse Mammary Tumor ◽  
Tumor Virus ◽  
Differential Gene

408. Liver gene expression in suckled postpartum beef cows maintained on moderate and improved subtropical pasture

2008 ◽  
Vol 20 (9) ◽  
pp. 88
Author(s):  
F. Samadi ◽  
H. M. Nadzir ◽  
N. J. Phillips ◽  
M. M. McGowan ◽  
SA Lehnert ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acid ◽  
Body Condition ◽  
Regulatory Element ◽  
Reproductive Function ◽  
Beef Cows ◽  
Binding Factor ◽  
Dairy Science ◽  
Sterol Regulatory Element ◽  
Hepatic Genes

The liver is the first organ to receive absorbed nutrients from the splanchnic vasculature1 which places the liver at an important juncture between nutrition, metabolic homeostasis and reproductive function. The best described component of this interface is secretion of IGF-1 by the liver and dependence of ovarian follicular maturation on hepatic-derived IGF-12. The aim in the present study was to ascertain the expression of hepatic genes associated with metabolic regulation in postpartum beef cows maintained on moderate or improved pasture, and with contrasting liveweight and body condition. Multiparous Droughtmaster cows (Bos taurus × Bos indicus) were placed on moderate (MP, n = 7) or improved (IP, n = 7) pasture at 6–7 months of gestation and remained on the treatments after calving. Liver biopsies were taken 6 weeks after calving and gene expression was determined by quantitative PCR using SYBR Green3. Week 6 represents attainment of the plateau in nutrient demand for lactation. Data were analysed by ANOVA using SAS STAT. One week after calving, IP cows had greater (P < 0.01) liveweight and body condition score (BCS) than MP cows (585 ± 12 kg and 528 ± 21 kg; 3.7 ± 0.2 BCS and 2.3 ± 0.2 BCS). IP cows had greater (P < 0.05) relative expression of hepatic genes associated with cholesterol biosynthesis (sterol regulatory element binding factor, SREBF2; peroxisome proliferators-activated receptor delta, PPARD), fatty acid biosynthesis (carnitine palmitoyl-transferase, CPT1A; acyl-CoA oxidase, ACOX1; fatty acid desaturase 1, FADS1; sterol regulatory element binding factor 1, SREBF1) and insulin signalling (hepatic insulin receptor substrate 1, IRS1). IP cows resumed cyclic ovarian function between 11–16 weeks postpartum and one MP cow had cycled by 16 weeks. The differences in expression of metabolic genes between MP and IP cows may have partly contributed to differences in reproductive function postpartum. (1) Drackley J et al. 2006 Journal of Dairy Science 89:1324–36 (2) Lucy MC 2000 Journal of Dairy Science 83:1635–47 (3) Loor JJ et al. 2006 Physiological Genomics 27:29–41

scholarly journals LSOSS: Detection of Cancer Outlier Differential Gene Expression

2010 ◽  
Vol 5 ◽  
pp. BMI.S5175 ◽  
Author(s):  
Yupeng Wang ◽  
Romdhane Rekaya
Keyword(s):  
Gene Expression ◽  
Differential Gene Expression ◽  
Profile Analysis ◽  
Gene Activation ◽  
Gene Signature ◽  
Human Breast ◽  
Disease Group ◽  
Activation Patterns ◽  
Cancer Data ◽  
Differential Gene

Detection of differential gene expression using microarray technology has received considerable interest in cancer research studies. Recently, many researchers discovered that oncogenes may be activated in some but not all samples in a given disease group. The existing statistical tools for detecting differentially expressed genes in a subset of the disease group mainly include cancer outlier profile analysis (COPA), outlier sum (OS), outlier robust t-statistic (ORT) and maximum ordered subset t-statistics (MOST). In this study, another approach named Least Sum of Ordered Subset Square t-statistic (LSOSS) is proposed. The results of our simulation studies indicated that LSOSS often has more power than previous statistical methods. When applied to real human breast and prostate cancer data sets, LSOSS was competitive in terms of the biological relevance of top ranked genes. Furthermore, a modified hierarchical clustering method was developed to classify the heterogeneous gene activation patterns of human breast cancer samples based on the significant genes detected by LSOSS. Three classes of gene activation patterns, which correspond to estrogen receptor (ER)+, ER– and a mixture of ER+ and ER–, were detected and each class was assigned a different gene signature.

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