The chromatin structure of specific genes: I. Evidence for higher order domains of defined DNA sequence

Wu, Carl; Bingham, Paul M.; Livak, Kenneth J.; Holmgren, Robert A.; Elgin, Sarah C. R.

doi:10.1016/0092-8674(79)90095-3

Cited by 436 publications

(180 citation statements)

References 15 publications

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“…In addition, It appears to require more than one specific sequence to fully anchor the actin gene to the matrix. Data from other laboratories have shown that there Is usually more than one hypersensitive site surrounding a transcriptionally active gene (22,(54)(55)(56)(57)(58)(59). It might be speculated that some of the proteins responsible for DNAase I hypersensitivity are also responsible for the matrix association of active genes.…”

Section: Resultsmentioning

confidence: 99%

The association of transcribed genes with the nuclear matrix ofDrosophilacells during heat shock

1985

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ABSIRACTUsing the transcriptional modulation afforded by heat shock, we found that the association of active genes with the nuclear matrix was not dependent on their level of transcription. Heat shock genes were matrix associated both before heat shock (when transcription was relatively low), and during heat shock (when transcription was greatly Increased). Conversely, the cytoplasmic actin gene was matrix associated during normal growth conditions (when transcription was high) and during heat shock (when transcription was greatly decreased). Removal of greater than 99.7% of nascent RNA during preparation of the matrices did not affect these findings. Detailed examination of the cytoplasmic actin gene revealed that Its matrix association was apparently mediated by multiple Interactions near the 5' end of the gene.

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Section: Resultsmentioning

confidence: 99%

The association of transcribed genes with the nuclear matrix ofDrosophilacells during heat shock

1985

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“…Transcriptional activation of this set of heat shock genes occurs within minutes of the temperature increase. Accompanying this activation are changes in chromosome structure that are evident from both the formation of puffs on polytene chromosomes (2) and the increased sensitivity of these genes to DNaseI in nuclei from heat shocked cells (3). However, the mechanistic relationships of these changes in structure to changes in gene expression remain to be established.…”

Section: Introductionmentioning

confidence: 99%

Two closely linked transcription units within the 63B heat shock puff locus of D. melanogaster display strikingly different regulation

O’Connor

Lis

1981

Nucl Acids Res

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We report the isolation and characterization of a cloned DNA of D. melanogaster, Dm4L, that is derived from the major heat shock puff site at 63B. This segment contains two closely linked genes that are each present once per Drosophila haploid genome. One of these, the hsp 83 gene, encodes an abundant heat shock mRNA that, unlike other major heat shock mRNAs, is also abundant in uninduced (230) Kco cells. Although only a slight increase in the level of total hsp 83 RNA can be detected after heat shock in Kco cells, the level of hsp 83 poly(A)+ mRNA increases more than 6-fold and the level of pulse-labeled hsp 83 RNA in total cellular RNA increases 11-fold relative to uninduced cells. In contrast, the levels of total, poly(A) , and pulselabeled RNA homologous to the second gene, 63B-T2, are approximately the same in both induced and uninduced cells. Hence, even though these genes are separated by only one thousand base pairs, and, from in situ hybridization to polytene chromosomes, both lie within the heat shock puff, they display strikingly different regulatory properties. These results demonstrate that close linkage of a gene to a heat shock puff is not sufficient to render its expression heat inducible.

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“…DNase I hypersensitivity analysis in S2 cells was performed as described in Wu et al (1979) with the following modifications. Nuclei were treated with 5 U/mL DNase I for 10 min, unless noted otherwise.…”

Section: Dnase I Hypersensitivity Analysismentioning

confidence: 99%

NELF-mediated stalling of Pol II can enhance gene expression by blocking promoter-proximal nucleosome assembly

Gilchrist¹,

Nechaev²,

Lee³

et al. 2008

Genes Dev.

282

298

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The Negative Elongation Factor (NELF) is a transcription regulatory complex that induces stalling of RNA polymerase II (Pol II) during early transcription elongation and represses expression of several genes studied to date, including Drosophila Hsp70, mammalian proto-oncogene junB, and HIV RNA. To determine the full spectrum of NELF target genes in Drosophila, we performed a microarray analysis of S2 cells depleted of NELF and discovered that NELF RNAi affects many rapidly inducible genes involved in cellular responses to stimuli. Surprisingly, only one-third of NELF target genes were, like Hsp70, up-regulated by NELF-depletion, whereas the majority of target genes showed decreased expression levels upon NELF RNAi. Our data reveal that the presence of stalled Pol II at this latter group of genes enhances gene expression by maintaining a permissive chromatin architecture around the promoter-proximal region, and that loss of Pol II stalling at these promoters is accompanied by a significant increase in nucleosome occupancy and a decrease in histone H3 Lys 4 trimethylation. These findings identify a novel, positive role for stalled Pol II in regulating gene expression and suggest that there is a dynamic interplay between stalled Pol II and chromatin structure.[Keywords: Gene expression; transcription elongation; polymerase stalling; chromatin structure] Supplemental material is available at http://www.genesdev.org.

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The chromatin structure of specific genes: I. Evidence for higher order domains of defined DNA sequence

Cited by 436 publications

References 15 publications

The association of transcribed genes with the nuclear matrix ofDrosophilacells during heat shock

The association of transcribed genes with the nuclear matrix ofDrosophilacells during heat shock

Two closely linked transcription units within the 63B heat shock puff locus of D. melanogaster display strikingly different regulation

NELF-mediated stalling of Pol II can enhance gene expression by blocking promoter-proximal nucleosome assembly

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