The mapping of nucleosomes and regulatory protein binding sites at the Saccharomyces cerevisiae MFA2 gene: a high resolution approach

Teng, Yumin; Yu, Shirong; Waters, Raymond

doi:10.1093/nar/29.13.e64

Cited by 18 publications

(25 citation statements)

References 18 publications

(25 reference statements)

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“…To test this idea, we examined the binding of TBP to the STE2 TATA box by ChIP and observed a strong increase in TBP occupancy in a cells, where this asg is active, relative to ␣ cells, where it is repressed (Fig. 2b), consistent with previous studies that probed the chromatin structure surrounding asg promoters (13,15,40,46,51,52,56,62,70). Thus, TBP is recruited to asg promoters after binding of the ␣2 repressor is lost.…”

Section: Resultssupporting

confidence: 84%

Corepressor-Directed Preacetylation of Histone H3 in Promoter Chromatin Primes Rapid Transcriptional Switching of Cell-Type-Specific Genes in Yeast

DeSimone

Laney

2010

Molecular and Cellular Biology

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Switching between alternate states of gene transcription is fundamental to a multitude of cellular regulatory pathways, including those that govern differentiation. In spite of the progress in our understanding of such transitions in gene activity, a major unanswered question is how cells regulate the timing of these switches. Here, we have examined the kinetics of a transcriptional switch that accompanies the differentiation of yeast cells of one mating type into a distinct new cell type. We found that cell-type-specific genes silenced by the ␣2 repressor in the starting state are derepressed to establish the new mating-type-specific gene expression program coincident with the loss of ␣2 from promoters. This rapid derepression does not require the preloading of RNA polymerase II or a preinitiation complex but instead depends upon the Gcn5 histone acetyltransferase. Surprisingly, Gcn5-dependent acetylation of nucleosomes in the promoters of mating-typespecific genes requires the corepressor Ssn6-Tup1 even in the repressed state. Gcn5 partially acetylates the amino-terminal tails of histone H3 in repressed promoters, thereby priming them for rapid derepression upon loss of ␣2. Thus, Ssn6-Tup1 not only efficiently represses these target promoters but also functions to initiate derepression by creating a chromatin state poised for rapid activation.Cells are dynamic entities. In response to the myriad signals that regulate cell growth, metabolism, and differentiation, cells have the remarkable ability to profoundly change their phenotype (7,30,43,55). Underlying such phenotypic switches are alterations in the expression programs of the cellular genome. These gene expression changes are regulated in large part at the level of gene transcription, requiring the combined action of sequence-specific DNA-binding factors and large multisubunit coregulatory complexes to trigger a transcriptional switch. While transcription factors directly bind to specific gene sets to change their transcriptional state, the coregulatory complexes are recruited and have more genome-wide roles as transcriptional adaptors, histone-modifying enzymes, chromatin-remodeling machines, and chromatin assembly/disassembly factors. Understanding how these cooperative assemblies interact with and respond to the signals that ultimately induce a phenotypic change is critical to producing a transcriptional switching event. Yet, despite intensive investigation, the molecular mechanisms that bring about such transitions in gene transcription remain only partially understood.A compelling model for understanding the mechanisms that regulate transcriptional switching events and the cellular phenotypic transitions they engender is the mating-type determination and switching system in the yeast Saccharomyces cerevisiae. This unicellular eukaryote can exist in two distinct haploid cell types called a and ␣. Each of these cell types displays a unique mating behavior; both are able to recognize and fuse with cells of the opposite type to form a diploid cell, but ne...

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Section: Resultssupporting

confidence: 84%

Corepressor-Directed Preacetylation of Histone H3 in Promoter Chromatin Primes Rapid Transcriptional Switching of Cell-Type-Specific Genes in Yeast

DeSimone

Laney

2010

Molecular and Cellular Biology

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“…We then radiolabelled and ran those fragments on alkaline agarose gels to identify any MNase protected regions at MFA2. If protected regions equivalent to lengths of about 147 base pairs are identified then this is an indication of the presence of a nucleosome in that region [16]. As shown in Fig.…”

Section: A Role For the Hat Gcn5 In Gg-nermentioning

confidence: 91%

“…In this review we will focus on work from our own groups, as other reviews in this edition are covering various additional aspects of how chromatin impinges on NER and the review by House et al [5] elegantly covers the broader aspects of this topic. We have had a long standing interest in yeast global genome NER [7][8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

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Histone modification and chromatin remodeling during NER

2015

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“…Histone acetylation enhances DNA repair, and S. cerevisiae gcn5Δ mutants are mildly sensitive to UV (46). In S. pombe, loss of Clr6 HDAC activity or deletion of its associated cofactors results in increased sensitivity to higher doses of UV (6).…”

Section: Molecular Cancer Therapeuticsmentioning

confidence: 99%

Inhibition of type I histone deacetylase increases resistance of checkpoint-deficient cells to genotoxic agents through mitotic delay

Alao

Olesch

Sunnerhagen

2009

Molecular Cancer Therapeutics

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Histone deacetylase (HDAC) inhibitors potently inhibit tumor growth and are currently being evaluated for their efficacy as chemosensitizers and radiosensitizers. This efficacy is likely to be limited by the fact that HDAC inhibitors also induce cell cycle arrest. Deletion of the class I HDAC Rpd3 has been shown to specifically suppress the sensitivity of Saccharomyces cerevisiae DNA damage checkpoint mutants to UV and hydroxyurea. We show that in the fission yeast Schizosaccharomyces pombe, inhibition of the homologous class I HDAC specifically suppresses the DNA damage sensitivity of checkpoint mutants. Importantly, the prototype HDAC inhibitor Trichostatin A also suppressed the sensitivity of DNA damage checkpoint but not of DNA repair mutants to UV and HU. TSA suppressed DNA damage activity independently of the mitogen-activated protein kinase-dependent and spindle checkpoint pathways. We show that TSA delays progression into mitosis and propose that this is the main mechanism for suppression of the DNA damage sensitivity of S. pombe checkpoint mutants, partially compensating for the loss of the G 2 checkpoint pathway. Our studies also show that the ability of HDAC inhibitors to suppress DNA damage sensitivity is not species specific. Class I HDACs are the major target of HDAC inhibitors and cancer cells are often defective in checkpoint activation. Effective use of these agents as chemosensitizers and radiosensitizers may require specific treatment schedules that circumvent their inhibition of cell cycle progression. [Mol Cancer Ther 2009;8(9):2606-15]

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The mapping of nucleosomes and regulatory protein binding sites at the Saccharomyces cerevisiae MFA2 gene: a high resolution approach

Cited by 18 publications

References 18 publications

Corepressor-Directed Preacetylation of Histone H3 in Promoter Chromatin Primes Rapid Transcriptional Switching of Cell-Type-Specific Genes in Yeast

Corepressor-Directed Preacetylation of Histone H3 in Promoter Chromatin Primes Rapid Transcriptional Switching of Cell-Type-Specific Genes in Yeast

Histone modification and chromatin remodeling during NER

Inhibition of type I histone deacetylase increases resistance of checkpoint-deficient cells to genotoxic agents through mitotic delay

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