Effect of transcription of yeast chromatin on DNA topology in vivo.

Pederson, David S.; Morse, Randall H.

doi:10.1002/j.1460-2075.1990.tb08313.x

Cited by 50 publications

(29 citation statements)

References 68 publications

(102 reference statements)

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“…It would be interesting to know whether the topological changes associated with transcription are behind this correlation. As the progression of the RNA polymerase through the DNA causes a change in superhelical density (Osborne and Guarentee, 1988;Brill and Sternglanz, 1988;Pederson and Morse, 1990;Lee and Garrad, 1991), it is likely that the shorter a gene is, the lower the change in superhelical density generated by transcription. Consequently the changes in supercoiling downstream of the RNA polymerase will be higher in long genes G+C content, ORF-length and mRNA concentration in S. cerevisiae 709 than in short genes.…”

Section: Discussionmentioning

confidence: 99%

Relationship between G+C content, ORF‐length and mRNA concentration in Saccharomyces cerevisiae

Marı́n

Gallardo

Kato

et al. 2003

Yeast

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RNA biogenesis is a tightly-regulated process. The levels and timing of expression of a gene depends on its particular function. However, gene expression levels may also depend on structural features. Here we describe the analysis of gene expression of 4977 ORFs using DNA microarrays covering the whole genome of three different S. cerevisiae strains, wild-type and tho2 and thp1 mutants with a general effect on mRNA biogenesis. We show that transcripts from G+C-rich ORFs accumulate at higher concentrations than those from G+C-poor ones, in different ORF-length categories in all strains tested. In addition, we found a negative correlation between ORF length and G+C content. Our results indicate that length and G+C content of a gene have a clear effect on its levels of expression. We discuss the biological relevance of these results, as well as different ways that these structural features could modulate mRNA biogenesis.

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Section: Discussionmentioning

confidence: 99%

Relationship between G+C content, ORF‐length and mRNA concentration in Saccharomyces cerevisiae

Marı́n

Gallardo

Kato

et al. 2003

Yeast

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“…Counts in the plasmid URA3 gene were compared with counts in the genomic ura3 gene by use of a Betagen imager. The copy number of each of the plasmids was found to be equal to each other and much lower than that required for the titration of HSF in yeast cells (31,50). This conclusion is further supported by genomic footprint analyses of control plasmid NPE-41 (see Fig.…”

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confidence: 81%

Heat shock factor can activate transcription while bound to nucleosomal DNA in Saccharomyces cerevisiae.

Pederson¹,

Fidrych²

1994

Mol. Cell. Biol.

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After each round of replication, new transcription initiation complexes must assemble on promoter DNA. This process may compete with packaging of the same promoter sequences into nucleosomes. To elucidate interactions between regulatory transcription factors and nucleosomes on newly replicated DNA, we asked whether heat shock factor (HSF) could be made to bind to nucleosomal DNA in vivo. A heat shock element (HSE) was embedded at either of two different sites within a DNA segment that directs the formation of a stable, positioned nucleosome. The resulting DNA segments were coupled to a reporter gene and transfected into the yeast Saccharomyces cerevisiae. Transcription from these two plasmid constructions after induction by heat shock was similar in amount to that from a control plasmid in which HSF binds to nucleosome-free DNA. High-resolution genomic footprint mapping of DNase I and micrococcal nuclease cleavage sites indicated that the HSE in these two plasmids was, nevertheless, packaged in a nucleosome. The inclusion of HSE sequences within (but relatively close to the edge of) the nucleosome did not alter the position of the nucleosome which formed with the parental DNA fragment. Genomic footprint analyses also suggested that the HSE-containing nucleosome was unchanged by the induction of transcription. Quantitative comparisons with control plasmids ruled out the possibility that HSF was bound only to a small fraction of molecules that might have escaped nucleosome assembly. Analysis of the helical orientation of HSE DNA in the nucleosome indicated that HSF contacted DNA residues that faced outward from the histone octamer. We discuss the significance of these results with regard to the role of nucleosomes in inhibiting transcription and the normal occurrence of nucleosome-free regions in promoters.After each round of replication, newly synthesized DNA must assemble with histones and transcription factors to form nucleosomes and transcription initiation complexes. 656-8749. assemble following DNA replication may not be naked DNA, but rather DNA that has already been organized by histones H3 and H4. This possibility suggests that some transcription factors, such as TFIIIA (25), can bind to or disrupt DNA-H3-H4 tetramers. Other factors may bind to or disrupt mature nucleosomes (reviewed in references 13, 22, 23, 53, and 58; see also reference 59). To the extent that this activity occurs in vivo, the assembly of a transcriptionally active promoter may not require the binding of transcription factors prior to nucleosome maturation.To further elucidate the in vivo mechanisms which govern the assembly of nucleosomes and transcription initiation complexes on newly replicated promoter DNA, we asked whether heat shock factor (HSF) can bind to DNA even if its target is contained within a nucleosome. Our in vivo competition experiments made use of synthetic promoters which present yeast cells with a choice among the binding of a regulatory factor to its DNA target, the assembly of that target into a nucleosome ...

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“…However, transcriptional activation can occur with minimal changes in DNA topology (Pederson & Morse 1990, Drabik et al 1997). This would be anticipated if histone acetylation was the only alteration to chromatin structure necessary for transcriptional activation.…”

Section: Chromatin Remodeling For Transcriptional Activation By Trmentioning

confidence: 99%

Nuclear receptors: coactivators, corepressors and chromatin remodeling in the control of transcription

Collingwood¹,

Fd²,

Ap³

1999

Journal of Molecular Endocrinology

294

172

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A contemporary view of hormone action at the transcriptional level requires knowledge of the transcription factors including the hormone receptor that may bind to promoters or enhancers, together with the chromosomal context within which these regulatory proteins function. Nuclear receptors provide the best examples of transcriptional control through the targeted recruitment of large protein complexes that modify chromosomal components and reversibly stabilize or destabilize chromatin. Ligand-dependent recruitment of transcriptional coactivators destabilizes chromatin by mechanisms including histone acetylation and contacts with the basal transcriptional machinery. In contrast, the recruitment of corepressors in the absence of ligand or in the presence of hormone antagonists serves to stabilize chromatin by the targeting of histone deacetylases. Both activation and repression require the action of other chromatin remodeling engines of the switch 2/sucrose nonfermentable 2 (SWI2/SNF2) class. Here we summarize this information and integrate hormone action into a chromatin context. Journal of Molecular Endocrinology (1999) 23, 255-275 INTRODUCTIONThe nuclear hormone receptors provide transcription research with a clear example of how the reversible modification of chromatin structure can contribute to the control of gene expression. Remarkable progress in the definition of intermediary protein complexes that activate or repress transcription has allowed common themes in transcriptional control by a wide variety of receptors to emerge. The roles of these coactivators and corepressors in mediating the activities of nuclear receptors within chromatin is a key element of contemporary molecular endocrinology. The beststudied receptors in this regard are those for the glucocorticoid and thyroid hormones.The glucocorticoid receptor recognizes response elements within nucleosomes as a first step towards a finely orchestrated rearrangement of histone-DNA contacts concomitant with the assembly of a functional transcription complex. The determinants of chromatin remodeling and the molecular machines that carry it out are now understood in considerable detail. Likewise, the thyroid hormone receptor recognizes nucleosomal DNA and utilizes chromatin to regulate transcription. However, in this case the receptor exerts a dual function. In the absence of ligand, the thyroid hormone receptor recruits a corepressor complex that stabilizes chromatin structure. Upon addition of hormone the receptor releases this repressive complex, and recruits coactivators that destabilize chromatin and promote transcription.This review illustrates the role of chromatin, coactivators and corepressors in gene control as orchestrated by the glucocorticoid and thyroid hormone receptors. COACTIVATORS AND COREPRESSORS CoactivatorsThe interplay of distinct nuclear receptor responsive transcription pathways has been recognized for 255

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Effect of transcription of yeast chromatin on DNA topology in vivo.

Cited by 50 publications

References 68 publications

Relationship between G+C content, ORF‐length and mRNA concentration in Saccharomyces cerevisiae

Relationship between G+C content, ORF‐length and mRNA concentration in Saccharomyces cerevisiae

Heat shock factor can activate transcription while bound to nucleosomal DNA in Saccharomyces cerevisiae.

Nuclear receptors: coactivators, corepressors and chromatin remodeling in the control of transcription

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