scholarly journals Autoregulation of fos: the dyad symmetry element as the major target of repression.

1989 ◽  
Vol 8 (9) ◽  
pp. 2559-2566 ◽  
Author(s):  
H. König ◽  
H. Ponta ◽  
U. Rahmsdorf ◽  
M. Büscher ◽  
A. Schönthal ◽  
...  
Keyword(s):  
Symmetry Element ◽  
Dyad Symmetry ◽  
Major Target

Mutation of the c-fos gene dyad symmetry element inhibits serum inducibility of transcription in vivo and the nuclear regulatory factor binding in vitro

1987 ◽  
Vol 7 (3) ◽  
pp. 1217-1225
Author(s):  
M E Greenberg ◽  
Z Siegfried ◽  
E B Ziff
Keyword(s):  
Growth Factor ◽  
Nuclear Protein ◽  
Symmetry Element ◽  
Regulatory Sequence ◽  
In Vitro Mutagenesis ◽  
Regulatory Factor ◽  
Mobility Shift ◽  
Sequence Element ◽  
Dyad Symmetry

In vitro mutagenesis of a 61-base-pair DNA sequence element that is necessary for induction of the c-fos proto-oncogene by growth factors revealed that a small region of dyad symmetry within the sequence element is critical for c-fos transcriptional activation. The same c-fos dyad symmetry element was found to bind a nuclear protein in vitro, causing a specific mobility shift of this c-fos regulatory sequence. An analysis of insertion and deletion mutants established a strict correlation between the ability of the dyad symmetry element to promote serum activation of c-fos transcription and in vitro nuclear protein binding. These experiments suggest that the DNA mobility shift assay detects a nuclear protein that mediates growth factor stimulation of c-fos expression. In vitro competition experiments indicate that the c-fos regulatory factor also binds to sequences within another growth factor-inducible gene, the beta-actin gene.

scholarly journals The dyad symmetry element is the molecular target for c-fos induction and inhibition during K 562 differentiation along mutually exclusive lineages

Blood ◽  
1991 ◽  
Vol 77 (1) ◽  
pp. 55-63 ◽  
Author(s):  
D Trouche ◽  
P Robin ◽  
P Sassone-Corsi ◽  
WL Farrar ◽  
A Harel-Bellan
Keyword(s):  
Transcriptional Activation ◽  
Regulatory Element ◽  
Regulatory Region ◽  
Myeloid Cell ◽  
Leukemic Cell ◽  
Erythroid Differentiation ◽  
Symmetry Element ◽  
Differentiation Markers ◽  
K 562 Cells ◽  
Dyad Symmetry

Abstract The c-fos proto-oncogene seems to play an important role during differentiation and activation of cells from the hematopoietic lineage. Therefore, it is of interest to investigate the mechanism underlying its transcriptional activation in these cells. To delineate the sequences and factors involved in c-fos transcriptional activation during the course of myeloid cell differentiation, we have used the K 562 chronic leukemic cell line as a model. K 562 cells were transfected with chloramphenicol transacetylase (CAT) reporter constructs, including various regions of the human c-fos promoter, and induced to differentiate by two distinct agents: 12-O-tetradecanoyl phorbol-13- acetate (TPA), which activates a differentiation program along the megakaryoblastic pathway; and hemin, which induces erythroid differentiation. We show here that TPA treatment of K 562 cells induces fos CAT reporter constructs activation, whereas treatment with hemin does not. Furthermore, predifferentiation of the cells with hemin blocks a subsequent induction by TPA, in correlation with the inhibition by hemin of megakaryoblastic differentiation markers appearance. Both the induction by TPA and the inhibition by hemin are mediated by a dyad symmetry element (DSE) located in the upstream regulatory region, between -318 and -296. These results suggest that the protein complex binding to the DSE regulatory element is the target for c-fos activation by TPA and inhibition by hemin in K 562 cells. However, no modulation of protein affinity for the DSE sequence was detected by gel shift assay during the course of induction or inhibition, suggesting that the structural change responsible for the transcriptional modulation is too unstable or too subtle to be detected by this method.

scholarly journals The dyad symmetry element is the molecular target for c-fos induction and inhibition during K 562 differentiation along mutually exclusive lineages

Blood ◽  
1991 ◽  
Vol 77 (1) ◽  
pp. 55-63
Author(s):  
D Trouche ◽  
P Robin ◽  
P Sassone-Corsi ◽  
WL Farrar ◽  
A Harel-Bellan
Keyword(s):  
Transcriptional Activation ◽  
Regulatory Element ◽  
Regulatory Region ◽  
Myeloid Cell ◽  
Leukemic Cell ◽  
Erythroid Differentiation ◽  
Symmetry Element ◽  
Differentiation Markers ◽  
K 562 Cells ◽  
Dyad Symmetry

The c-fos proto-oncogene seems to play an important role during differentiation and activation of cells from the hematopoietic lineage. Therefore, it is of interest to investigate the mechanism underlying its transcriptional activation in these cells. To delineate the sequences and factors involved in c-fos transcriptional activation during the course of myeloid cell differentiation, we have used the K 562 chronic leukemic cell line as a model. K 562 cells were transfected with chloramphenicol transacetylase (CAT) reporter constructs, including various regions of the human c-fos promoter, and induced to differentiate by two distinct agents: 12-O-tetradecanoyl phorbol-13- acetate (TPA), which activates a differentiation program along the megakaryoblastic pathway; and hemin, which induces erythroid differentiation. We show here that TPA treatment of K 562 cells induces fos CAT reporter constructs activation, whereas treatment with hemin does not. Furthermore, predifferentiation of the cells with hemin blocks a subsequent induction by TPA, in correlation with the inhibition by hemin of megakaryoblastic differentiation markers appearance. Both the induction by TPA and the inhibition by hemin are mediated by a dyad symmetry element (DSE) located in the upstream regulatory region, between -318 and -296. These results suggest that the protein complex binding to the DSE regulatory element is the target for c-fos activation by TPA and inhibition by hemin in K 562 cells. However, no modulation of protein affinity for the DSE sequence was detected by gel shift assay during the course of induction or inhibition, suggesting that the structural change responsible for the transcriptional modulation is too unstable or too subtle to be detected by this method.

scholarly journals Mutation of the c-fos gene dyad symmetry element inhibits serum inducibility of transcription in vivo and the nuclear regulatory factor binding in vitro.

1987 ◽  
Vol 7 (3) ◽  
pp. 1217-1225 ◽  
Author(s):  
M E Greenberg ◽  
Z Siegfried ◽  
E B Ziff
Keyword(s):  
Growth Factor ◽  
Nuclear Protein ◽  
Symmetry Element ◽  
Regulatory Sequence ◽  
In Vitro Mutagenesis ◽  
Regulatory Factor ◽  
Mobility Shift ◽  
Sequence Element ◽  
Dyad Symmetry

In vitro mutagenesis of a 61-base-pair DNA sequence element that is necessary for induction of the c-fos proto-oncogene by growth factors revealed that a small region of dyad symmetry within the sequence element is critical for c-fos transcriptional activation. The same c-fos dyad symmetry element was found to bind a nuclear protein in vitro, causing a specific mobility shift of this c-fos regulatory sequence. An analysis of insertion and deletion mutants established a strict correlation between the ability of the dyad symmetry element to promote serum activation of c-fos transcription and in vitro nuclear protein binding. These experiments suggest that the DNA mobility shift assay detects a nuclear protein that mediates growth factor stimulation of c-fos expression. In vitro competition experiments indicate that the c-fos regulatory factor also binds to sequences within another growth factor-inducible gene, the beta-actin gene.

scholarly journals Specific Methylation Patterns in Two Control Regions of Epstein-Barr Virus Latency: the LMP-1-Coding Upstream Regulatory Region and an Origin of DNA Replication (oriP)

1998 ◽  
Vol 72 (4) ◽  
pp. 2969-2974 ◽  
Author(s):  
Kerstin I. Falk ◽  
Laszlo Szekely ◽  
Anna Aleman ◽  
Ingemar Ernberg
Keyword(s):  
Epstein Barr Virus ◽  
Methylation Status ◽  
Regulatory Region ◽  
Cell Types ◽  
Symmetry Element ◽  
Regulatory Sequence ◽  
Type I ◽  
Barr Virus ◽  
Epstein Barr ◽  
Dyad Symmetry

ABSTRACT The Epstein-Barr virus (EBV) can establish at least four different forms of latent infection. Previously, we have shown that the level of methylation of the EBV genome varies, depending on the form of latency. The methylation status of CpGs was analyzed by the bisulfite genomic sequencing technique in four different cell types representing different forms of latency. The dyad symmetry element of the origin of replication (oriP) region and the latent membrane protein 1 (LMP-1) regulatory sequence (LRS) were studied. The dyad symmetry element has four binding sites for EBNA-1. In a cell with type I latency, a region upstream of the dyad symmetry element was highly methylated, whereas the dyad symmetry element was unmethylated in the EBNA-1-binding region. The LRS was extensively methylated in the LMP-1-negative cell line Rael, in contrast to a LMP-1-expressing nasopharyngeal carcinoma tumor (NPC C15), which was almost completely unmethylated. The methylation pattern of LRS in type I and type III Burkitt lymphoma cells of similar parental origins confirmed that demethylation of some regions takes place upon phenotypic drift.

scholarly journals Rep*: a Viral Element That Can Partially Replace the Origin of Plasmid DNA Synthesis of Epstein-Barr Virus

1998 ◽  
Vol 72 (6) ◽  
pp. 4657-4666 ◽  
Author(s):  
Ann L. Kirchmaier ◽  
Bill Sugden
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Simian Virus 40 ◽  
Dominant Negative ◽  
Symmetry Element ◽  
Nuclear Antigen ◽  
Origin Of Replication ◽  
The Family ◽  
Epstein Barr ◽  
Dyad Symmetry

ABSTRACT Replication of the Epstein-Barr viral (EBV) genome occurs once per cell cycle during latent infection. Similarly, plasmids containing EBV’s plasmid origin of replication, oriP, are replicated once per cell cycle. Replication from oriP requires EBV nuclear antigen 1 (EBNA-1) in trans; however, its contributions to this replication are unknown. oriPcontains 24 EBNA-1 binding sites; 20 are located within the family of repeats, and 4 are found within the dyad symmetry element. The site of initiation of DNA replication within oriP is at or near the dyad symmetry element. We have identified a plasmid that contains the family of repeats but lacks the dyad symmetry element whose replication can be detected for a limited number of cell cycles. The detection of short-term replication of this plasmid requires EBNA-1 and can be inhibited by a dominant-negative inhibitor of EBNA-1. We have identified two regions within this plasmid which can independently contribute to this replication in the absence of the dyad symmetry element of oriP. One region contains native EBV sequences within the BamHI C fragment of the B95-8 genome of EBV; the other contains sequences within the simian virus 40 genome. We have mapped the region contributing to replication within the EBV sequences to a 298-bp fragment, Rep*. Plasmids which contain three copies of Rep* plus the family of repeats support replication more efficiently than those with one copy, consistent with a stochastic model for the initiation of DNA synthesis. Plasmids with three copies of Rep* also support long-term replication in the presence of EBNA-1. These observations together indicate that the latent origin of replication of EBV is more complex than formerly appreciated; it is a multicomponent origin of which the dyad symmetry element is one efficient component. The experimental approach described here could be used to identify eukaryotic sequences which mediate DNA synthesis, albeit inefficiently.

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