An initiation element in the yeast<i>CUP1</i>promoter is recognized by RNA polymerase II in the absence of TATA box-binding protein if the DNA is negatively supercoiled

LeBlanc, B.P.; Benham, Craig J.; Clark, David

doi:10.1073/pnas.200365097

Cited by 35 publications

(36 citation statements)

References 46 publications

(35 reference statements)

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“…Furthermore, Ace1p activates transcription independently of most of the TAFs (37). Thus, CUP1 appears to be an example of simplified regulation (27).…”

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confidence: 98%

Remodeling of YeastCUP1Chromatin Involves Activator-Dependent Repositioning of Nucleosomes over the Entire Gene and Flanking Sequences

Shen

LeBlanc

Alfieri

et al. 2001

Molecular and Cellular Biology

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The yeast CUP1 gene is activated by the copper-dependent binding of the transcriptional activator, Ace1p. An episome containing transcriptionally active or inactive CUP1 was purified in its native chromatin structure from yeast cells. The amount of RNA polymerase II on CUP1 in the purified episomes correlated with its transcriptional activity in vivo. Chromatin structures were examined by using the monomer extension technique to map translational positions of nucleosomes. The chromatin structure of an episome containing inactive CUP1 isolated from ace1⌬ cells is organized into clusters of overlapping nucleosome positions separated by linkers. Novel nucleosome positions that include the linkers are occupied in the presence of Ace1p. Repositioning was observed over the entire CUP1 gene and its flanking regions, possibly over the entire episome. Mutation of the TATA boxes to prevent transcription did not prevent repositioning, implicating a chromatin remodeling activity recruited by Ace1p. These observations provide direct evidence in vivo for the nucleosome sliding mechanism proposed for remodeling complexes in vitro and indicate that remodeling is not restricted to the promoter but occurs over a chromatin domain including CUP1 and its flanking sequences.

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“…Furthermore, Ace1p activates transcription independently of most of the TAFs (37). Thus, CUP1 appears to be an example of simplified regulation (27).…”

mentioning

confidence: 98%

Remodeling of YeastCUP1Chromatin Involves Activator-Dependent Repositioning of Nucleosomes over the Entire Gene and Flanking Sequences

Shen

LeBlanc

Alfieri

et al. 2001

Molecular and Cellular Biology

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“…Initiation of transcription from the human MYC proto-oncogene is regulated by the binding of FBP to the single-stranded DNA regulatory element FUSE (He et al 2000). The minimal conditions for in vitro transcriptional initiation from the yeast CUP1 (YHR053C) gene promoter are a negatively superhelical DNA substrate plus RNA polymerase (RNAP); no other regulatory molecules are required (Leblanc et al 2000). SIDD also has been implicated in transcriptional termination in yeast (Benham 1996;Aranda et al 1997).…”

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confidence: 99%

Stress-Induced DNA Duplex Destabilization (SIDD) in the E. coli Genome: SIDD Sites Are Closely Associated With Promoters

Wang¹,

Noordewier²,

Benham³

2004

Genome Res.

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We present the first analysis of stress-induced DNA duplex destabilization (SIDD) in a complete chromosome, the Escherichia coli K12 genome. We used a newly developed method to calculate the locations and extents of stress-induced destabilization to single-base resolution at superhelix density = −0.06. We find that SIDD sites in this genome show a statistically highly significant tendency to avoid coding regions. And among intergenic regions, those that either contain documented promoters or occur between divergently transcribing coding regions, and hence may be inferred to contain promoters, are associated with strong SIDD sites in a statistically highly significant manner. Intergenic regions located between convergently transcribing genes, which are inferred not to contain promoters, are not significantly enriched for destabilized sites. Statistical analysis shows that a strongly destabilized intergenic region has an 80% chance of containing a promoter, whereas an intergenic region that does not contain a strong SIDD site has only a 24% chance. We describe how these observations may illuminate specific mechanisms of regulation, and assist in the computational identification of promoter locations in prokaryotes.Because the initiation of transcription and the initiation of replication both require local separation of the DNA duplex, the locations and occasions where this transition occurs in vivo must be stringently controlled. One biologically important way in which local DNA stability is regulated is through superhelical stresses imposed on the duplex (Benham 1979). Negative DNA superhelicity exerts untwisting torsional stresses on the base pairs that experience it. When these stresses are sufficiently large, they can drive local structural transitions to conformations whose right-handed helicities are less than that of the B-form (Benham 1981). Because strand separation locally unwinds the DNA, it localizes some of the imposed superhelicity, which relaxes by a corresponding amount the level of stress on the rest of the domain. Thus the free energy cost of this transition is partially or fully offset by the free energy returned from the fractional relaxation it provides. When this return exceeds its cost, a transition will be favored at equilibrium.Local sites of strand separation (also called local denaturation, duplex opening, or unwinding), the most extreme form of duplex destabilization, can be induced by moderate levels of negative superhelicity (Benham 1980;Kowalski et al. 1988;Lyubchenko and Shlyakhtenko 1988;Voloshin et al. 1989). Partial destabilizations also can occur, in which the imposed superhelical stresses fractionally decrease the free energy needed to separate the duplex. Partial destabilization can be biologically important, as it decreases the amount of free energy other molecules must provide to drive separation at the site involved, and hence can facilitate regulatory events.The relaxation induced by strand separation at any one site is felt by all other base pairs, and their propensities ...

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“…Ace1p activates transcription through its C-terminal acidic activation domain. The CUP1 promoter contains two consensus TATA boxes (10) and an initiation element (24). CUP1 is also induced relatively weakly by heat shock, mediated via the binding of heat shock factor to sites in the CUP1 promoter (29).…”

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confidence: 99%

Targeted Histone Acetylation at the Yeast CUP1 Promoter Requires the Transcriptional Activator, the TATA Boxes, and the Putative Histone Acetylase Encoded by SPT10

Shen

LeBlanc

Neal

et al. 2002

Molecular and Cellular Biology

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The relationship between chromatin remodeling and histone acetylation at the yeast CUP1 gene was addressed. CUP1 encodes a metallothionein required for cell growth at high copper concentrations. Induction of CUP1 with copper resulted in targeted acetylation of both H3 and H4 at the CUP1 promoter. Nucleosomes containing upstream activating sequences and sequences farther upstream were the targets for H3 acetylation. Targeted acetylation of H3 and H4 required the transcriptional activator (Ace1p) and the TATA boxes, suggesting that targeted acetylation occurs when TATA-binding protein binds to the TATA box or at a later stage in initiation. We have shown previously that induction results in nucleosome repositioning over the entire CUP1 gene, which requires Ace1p but not the TATA boxes. Therefore, the movement of nucleosomes occurring on CUP1 induction is independent of targeted acetylation. Targeted acetylation of both H3 and H4 also required the product of the SPT10 gene, which encodes a putative histone acetylase implicated in regulation at core promoters. Disruption of SPT10 was lethal at high copper concentrations and correlated with slower induction and reduced maximum levels of CUP1 mRNA. These observations constitute evidence for a novel mechanism of chromatin activation at CUP1, with a major role for the TATA box.Eukaryotic DNA is packaged into the cell nucleus in the form of chromatin. The basic structural repeat unit of chromatin is the nucleosome, in which 147 bp of DNA are wrapped in nearly two superhelical turns around a central core histone octamer that is composed of two molecules each of the four core histones H2A, H2B, H3, and H4. A molecule of histone H1 is bound to the nucleosome core and to the linker DNA and directs the folding of the chromatin fiber. The assembly of DNA into nucleosomes represses transcription in vitro, raising the question of how the cell copes with chromatin. It is now clear that chromatin structure is more than just a DNA packaging system: it is intimately connected with events in gene regulation. This is evident from the identification of two classes of chromatin-modifying activities (17,43,48): (i) remodeling complexes, which use the energy of ATP hydrolysis to effect changes in chromatin structure, and (ii) histone modifying complexes, which modify histones posttranslationally (notably, histone acetyltransferases [HATs] and deacetylases

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An initiation element in the yeastCUP1promoter is recognized by RNA polymerase II in the absence of TATA box-binding protein if the DNA is negatively supercoiled

Cited by 35 publications

References 46 publications

Remodeling of YeastCUP1Chromatin Involves Activator-Dependent Repositioning of Nucleosomes over the Entire Gene and Flanking Sequences

Remodeling of YeastCUP1Chromatin Involves Activator-Dependent Repositioning of Nucleosomes over the Entire Gene and Flanking Sequences

Stress-Induced DNA Duplex Destabilization (SIDD) in the E. coli Genome: SIDD Sites Are Closely Associated With Promoters

Targeted Histone Acetylation at the Yeast CUP1 Promoter Requires the Transcriptional Activator, the TATA Boxes, and the Putative Histone Acetylase Encoded by SPT10

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