scholarly journals Serum stimulation of the c-fos enhancer induces reversible changes in c-fos chromatin structure.

1990 ◽  
Vol 10 (3) ◽  
pp. 1126-1133 ◽  
Author(s):  
J L Feng ◽  
B Villeponteau
Keyword(s):  
Growth Factors ◽  
Dna Sequences ◽  
Chromatin Structure ◽  
Transcriptional Activity ◽  
Dnase I ◽  
Enhancer Activity ◽  
Serum Stimulation ◽  
Fos Protein ◽  
Dnase I Sensitivity ◽  
Stimulation Of

Transcription of the proto-oncogene c-fos is known to be activated by growth factors in serum and subsequently repressed by the Fos protein. We show that generalized DNase I sensitivity of c-fos chromatin correlates closely with enhancer activity during induction, repression, and superinduction of the c-fos gene. Within 90 s of serum stimulation, proximal DNA sequences on both sides of the enhancer exhibit increased DNase I sensitivity. Within 5 min, elevated DNase I sensitivity spreads to chromatin at the distal 3' end of the c-fos gene. These results suggest that an open state of chromatin is propagated in both directions from the enhancer. The induced alterations in chromatin structure precede the increased transcriptional activity of the c-fos gene, suggesting that these changes in chromatin structure potentiate transcription.

Serum stimulation of the c-fos enhancer induces reversible changes in c-fos chromatin structure

1990 ◽  
Vol 10 (3) ◽  
pp. 1126-1133
Author(s):  
J L Feng ◽  
B Villeponteau
Keyword(s):  
Growth Factors ◽  
Dna Sequences ◽  
Chromatin Structure ◽  
Transcriptional Activity ◽  
Dnase I ◽  
Enhancer Activity ◽  
Serum Stimulation ◽  
Fos Protein ◽  
Dnase I Sensitivity ◽  
Stimulation Of

Transcription of the proto-oncogene c-fos is known to be activated by growth factors in serum and subsequently repressed by the Fos protein. We show that generalized DNase I sensitivity of c-fos chromatin correlates closely with enhancer activity during induction, repression, and superinduction of the c-fos gene. Within 90 s of serum stimulation, proximal DNA sequences on both sides of the enhancer exhibit increased DNase I sensitivity. Within 5 min, elevated DNase I sensitivity spreads to chromatin at the distal 3' end of the c-fos gene. These results suggest that an open state of chromatin is propagated in both directions from the enhancer. The induced alterations in chromatin structure precede the increased transcriptional activity of the c-fos gene, suggesting that these changes in chromatin structure potentiate transcription.

scholarly journals Microinjection of transforming ras protein induces c-fos expression.

1987 ◽  
Vol 7 (1) ◽  
pp. 523-527 ◽  
Author(s):  
D W Stacey ◽  
T Watson ◽  
H F Kung ◽  
T Curran
Keyword(s):  
Protein Accumulation ◽  
3T3 Cells ◽  
Ras Protein ◽  
Serum Stimulation ◽  
Fos Protein ◽  
Fos Expression ◽  
High Level ◽  
Stimulation Of

Microinjection of p21ras induced c-fos protein accumulation in three types of 3T3 cells. The induction was rapid and efficient and persisted for many hours. In addition, anti-ras antibody dramatically reduced c-fos accumulation after serum stimulation of injected cells. However, cells which expressed p21ras continuously did not maintain a high level of c-fos expression.

scholarly journals Widespread Collaboration of Isw2 and Sin3-Rpd3 Chromatin Remodeling Complexes in Transcriptional Repression

2001 ◽  
Vol 21 (19) ◽  
pp. 6450-6460 ◽  
Author(s):  
Thomas G. Fazzio ◽  
Charles Kooperberg ◽  
Jesse P. Goldmark ◽  
Cassandra Neal ◽  
Ryan Basom ◽  
...  
Keyword(s):  
Chromatin Remodeling ◽  
Chromatin Structure ◽  
Transcriptional Repression ◽  
Target Genes ◽  
Full Range ◽  
Dnase I ◽  
Genome Expression ◽  
Complex Functions ◽  
Dnase I Sensitivity ◽  
Chromatin Remodeling Complexes

ABSTRACT The yeast Isw2 chromatin remodeling complex functions in parallel with the Sin3-Rpd3 histone deacetylase complex to repress early meiotic genes upon recruitment by Ume6p. For many of these genes, the effect of an isw2 mutation is partially masked by a functional Sin3-Rpd3 complex. To identify the full range of genes repressed or activated by these factors and uncover hidden targets of Isw2-dependent regulation, we performed full genome expression analyses using cDNA microarrays. We find that the Isw2 complex functions mainly in repression of transcription in a parallel pathway with the Sin3-Rpd3 complex. In addition to Ume6 target genes, we find that many Ume6-independent genes are derepressed in mutants lacking functional Isw2 and Sin3-Rpd3 complexes. Conversely, we find thatume6 mutants, but not isw2 sin3 or isw2 rpd3 double mutants, have reduced fidelity of mitotic chromosome segregation, suggesting that one or more functions of Ume6p are independent of Sin3-Rpd3 and Isw2 complexes. Chromatin structure analyses of two nonmeiotic genes reveals increased DNase I sensitivity within their regulatory regions in an isw2 mutant, as seen previously for one meiotic locus. These data suggest that the Isw2 complex functions at Ume6-dependent and -independent loci to create DNase I-inaccessible chromatin structure by regulating the positioning or placement of nucleosomes.

scholarly journals The jun and fos protein families are both required for cell cycle progression in fibroblasts.

1991 ◽  
Vol 11 (9) ◽  
pp. 4466-4472 ◽  
Author(s):  
K Kovary ◽  
R Bravo
Keyword(s):  
Cell Cycle ◽  
Transcription Factors ◽  
Dna Synthesis ◽  
Cell Cycle Progression ◽  
S Phase ◽  
3T3 Cells ◽  
Cycle Progression ◽  
Serum Stimulation ◽  
Fos Protein ◽  
Stimulation Of

The expression of different members of the Jun and Fos families of transcription factors is rapidly induced following serum stimulation of quiescent fibroblasts. To determine whether these proteins are required for cell cycle progression, we microinjected affinity-purified antibodies directed against c-Fos, FosB, Fra-1, c-Jun, JunB, and JunD, and antibodies that recognize either the Fos or the Jun family of proteins, into Swiss 3T3 cells and determined their effects in cell cycle progression by monitoring DNA synthesis. We found that microinjection of anti-Fos and anti-Jun family antibodies efficiently blocked the entrance to the S phase of serum-stimulated or asynchronously growing cells. However, the antibodies against single members of the Fos family only partially inhibited DNA synthesis. In contrast, all three Jun antibodies prevented DNA synthesis more effectively than did any of the anti-Fos antibodies.

Chromatin structure of the HLA-DR alpha gene in different functional states of major histocompatibility complex class II gene expression

1987 ◽  
Vol 7 (5) ◽  
pp. 1967-1972
Author(s):  
B M Peterlin ◽  
K J Hardy ◽  
A S Larsen
Keyword(s):  
Dna Sequences ◽  
Chromatin Structure ◽  
Gene Promoter ◽  
Dnase I ◽  
Consensus Sequences ◽  
Histocompatibility Complex ◽  
Hla Dr ◽  
Hypersensitive Sites ◽  
Alpha Gene ◽  
Regulatory Loci

We utilized DNase I hypersensitivity mapping to study chromatin structure within the HLA-DR alpha gene. We found a single DNase I-hypersensitive site coinciding with the HLA-DR alpha gene promoter in all cells studied. Moreover, in cells that constitutively express HLA-DR, two additional DNase I-hypersensitive sites were observed. These lie within the first intron of the HLA-DR alpha gene and encompass DNA sequences that share homologies with regulatory loci of the immunoglobulin and immune response genes, as well as with core enhancer consensus sequences.

Microinjection of transforming ras protein induces c-fos expression

1987 ◽  
Vol 7 (1) ◽  
pp. 523-527
Author(s):  
D W Stacey ◽  
T Watson ◽  
H F Kung ◽  
T Curran
Keyword(s):  
Protein Accumulation ◽  
3T3 Cells ◽  
Ras Protein ◽  
Serum Stimulation ◽  
Fos Protein ◽  
Fos Expression ◽  
High Level ◽  
Stimulation Of

Microinjection of p21ras induced c-fos protein accumulation in three types of 3T3 cells. The induction was rapid and efficient and persisted for many hours. In addition, anti-ras antibody dramatically reduced c-fos accumulation after serum stimulation of injected cells. However, cells which expressed p21ras continuously did not maintain a high level of c-fos expression.

scholarly journals Chromatin structure of the HLA-DR alpha gene in different functional states of major histocompatibility complex class II gene expression.

1987 ◽  
Vol 7 (5) ◽  
pp. 1967-1972 ◽  
Author(s):  
B M Peterlin ◽  
K J Hardy ◽  
A S Larsen
Keyword(s):  
Dna Sequences ◽  
Chromatin Structure ◽  
Gene Promoter ◽  
Dnase I ◽  
Consensus Sequences ◽  
Histocompatibility Complex ◽  
Hla Dr ◽  
Hypersensitive Sites ◽  
Alpha Gene ◽  
Regulatory Loci

We utilized DNase I hypersensitivity mapping to study chromatin structure within the HLA-DR alpha gene. We found a single DNase I-hypersensitive site coinciding with the HLA-DR alpha gene promoter in all cells studied. Moreover, in cells that constitutively express HLA-DR, two additional DNase I-hypersensitive sites were observed. These lie within the first intron of the HLA-DR alpha gene and encompass DNA sequences that share homologies with regulatory loci of the immunoglobulin and immune response genes, as well as with core enhancer consensus sequences.

scholarly journals Role of the Promoter in Maintaining Transcriptionally Active Chromatin Structure and DNA Methylation Patterns In Vivo

2003 ◽  
Vol 23 (12) ◽  
pp. 4150-4161 ◽  
Author(s):  
Sung-Hae Lee Kang ◽  
Christine Mione Kiefer ◽  
Thomas P. Yang
Keyword(s):  
Dna Methylation ◽  
Chromatin Structure ◽  
Dnase I ◽  
Dnase I Hypersensitivity ◽  
Translation Start ◽  
Dnase I Sensitivity ◽  
Active Transcription ◽  
Methylation Patterns

ABSTRACT Establishment and maintenance of differential chromatin structure between transcriptionally competent and repressed genes are critical aspects of transcriptional regulation. The elements and mechanisms that mediate formation and maintenance of these chromatin states in vivo are not well understood. To examine the role of the promoter in maintaining chromatin structure and DNA methylation patterns of the transcriptionally active X-linked HPRT locus, 323 bp of the endogenous human HPRT promoter (from position −222 to +102 relative to the translation start site) was replaced by plasmid sequences by homologous recombination in cultured HT-1080 male fibrosarcoma cells. The targeted cells, which showed no detectable HPRT transcription, were then assayed for effects on DNase I hypersensitivity, general DNase I sensitivity, and DNA methylation patterns across the HPRT locus. In cells carrying the deletion, significantly diminished DNase I hypersensitivity in the 5′ flanking region was observed compared to that in parental HT-1080 cells. However, general DNase I sensitivity and DNA methylation patterns were found to be very similar in the mutated cells and in the parental cells. These findings suggest that the promoter and active transcription play a relatively limited role in maintaining transcriptionally potentiated epigenetic states.

Transcriptional activation of mammalian ornithine decarboxylase during stimulated growth

1987 ◽  
Vol 7 (7) ◽  
pp. 2641-2643
Author(s):  
A Katz ◽  
C Kahana
Keyword(s):  
Protein Synthesis ◽  
Growth Factors ◽  
Ornithine Decarboxylase ◽  
Transcriptional Activation ◽  
Tumor Promoter ◽  
Transcriptional Analysis ◽  
Mouse Fibroblasts ◽  
Serum Stimulation ◽  
Stimulation Of

Cloned ornithine decarboxylase (ODC) (EC 4.1.1.17) cDNA was used to investigate the mechanisms which mediate the mitogenic induction of mammalian ODC. Stimulation of quiescent BALB/c 3T3 mouse fibroblasts with purified fibroblast and platelet-derived growth factors and with the tumor promoter 12-O-tetradecanoylphorbol-13-acetate results in a rapid and dramatic increase in ODC mRNA, similar to the increase caused by serum stimulation. Using nuclear runoff transcriptional analysis, we demonstrate that an increase in ODC transcription accounts for the mitogenic induction of ODC mRNA, and using cycloheximide together with the stimulating mitogen, we found that the mitogenic induction of ODC is dependent on ongoing protein synthesis in the stimulated cells.

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