Stress-Dependent Dynamics of Global Chromatin Remodeling in Yeast: Dual Role for SWI/SNF in the Heat Shock Stress Response

Shivaswamy, Sushma; Iyer, Vishwanath R.

doi:10.1128/mcb.01659-07

Cited by 128 publications

(120 citation statements)

References 61 publications

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“…Affected genes do not fall into particular functional categories, although these data led to the discovery that Swi/Snf function is important for transcription during M phase (Krebs et al 2000). More recently, analysis of the heat-shock response showed that Swi/Snf directly regulates both ribosomal protein genes and genes under the control of heat-shock factor (Shivaswamy and Iyer 2008). These microarray studies likely underestimate the extent to which Swi/Snf controls transcription, as few conditions were tested.…”

Section: Regulation Of Transcription By Swi/snfmentioning

confidence: 99%

Chromatin and Transcription in Yeast

2012

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Understanding the mechanisms by which chromatin structure controls eukaryotic transcription has been an intense area of investigation for the past 25 years. Many of the key discoveries that created the foundation for this field came from studies of Saccharomyces cerevisiae, including the discovery of the role of chromatin in transcriptional silencing, as well as the discovery of chromatin-remodeling factors and histone modification activities. Since that time, studies in yeast have continued to contribute in leading ways. This review article summarizes the large body of yeast studies in this field.

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Section: Regulation Of Transcription By Swi/snfmentioning

confidence: 99%

Chromatin and Transcription in Yeast

2012

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“…The two remodelers have very different binding distributions through the genome, with INO80 mapping to replication origins, tRNA genes, and a subset of RNA PolII promoters (Shimada et al 2008). Snf2 is present at high levels in ribosomal protein genes (Shivaswamy and Iyer 2008). Recent work has argued that INO80 preferentially exchanges Htz1-containing nucleosomes for canonical H2A/H2B dimers (PapamichosChronakis et al 2011), while SWI/SNF does not.…”

Section: The Mechanism Of Chromatin Movementmentioning

confidence: 99%

Targeted INO80 enhances subnuclear chromatin movement and ectopic homologous recombination

Neumann¹,

Dion²,

Gehlen³

et al. 2012

Genes Dev.

162

221

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Chromatin in the interphase nucleus moves in a constrained random walk. Despite extensive study, the molecular causes of such movement and its impact on DNA-based reactions are unclear. Using high-precision live fluorescence microscopy in budding yeast, we quantified the movement of tagged chromosomal loci to which transcriptional activators or nucleosome remodeling complexes were targeted. We found that local binding of the transcriptional activator VP16, but not of the Gal4 acidic domain, enhances chromatin mobility. The increase in movement did not correlate strictly with RNA polymerase II (PolII) elongation, but could be phenocopied by targeting the INO80 remodeler to the locus. Enhanced chromatin mobility required Ino80's ATPase activity. Consistently, the INO80-dependent remodeling of nucleosomes upon transcriptional activation of the endogenous PHO5 promoter enhanced chromatin movement locally. Finally, increased mobility at a double-strand break was also shown to depend in part on the INO80 complex. This correlated with increased rates of spontaneous gene conversion. We propose that local chromatin remodeling and nucleosome eviction increase large-scale chromatin movements by enhancing the flexibility of the chromatin fiber.[Keywords: chromatin remodeling; nuclear organization; transcription; VP16; Ino80; fluorescence microscopy; homologous recombination] Supplemental material is available for this article.Received August 15, 2011; revised version accepted January 13, 2012.DNA-based transactions such as transcription, replication, and repair take place in distinct nuclear subcompartments. Transcriptional silencing is frequently associated with the nuclear envelope or occurs near nucleoli (Towbin et al. 2009), whereas the activation of tissue-specific genes correlates with a shift of the relevant genes away from the nuclear periphery (Egecioglu and Brickner 2011). In contrast, genes activated under conditions of nutrient or temperature stress move to nuclear pores when they are induced (Taddei 2007). Finally, some types of damagenamely, irreparable DNA double-strand breaks (DSBs), collapsed replication forks, and eroded telomeres-relocate to nuclear pores to be processed for repair, unlike DSBs that can be repaired by recombination with a homologous template (for review, see Nagai et al. 2010). For these relocalization events to occur, whether at a promoter, a replication fork, or a DSB, chromatin must be mobile.Rapid time-lapse fluorescence microscopy of GFP-LacItagged genomic loci has shown that individual chromosomal domains move constantly in a near-random walk within a restrained volume of the nucleus (Hubner and Spector 2010). The measured radius of constraint for the movement of an average chromosomal locus (;0.6 mm) was roughly similar in every species investigated, although mobility was also shown to be influenced by local chromatin context (Marshall et al. 1997;Heun et al. 2001;Vazquez et al. 2001;Chubb et al. 2002;Gartenberg et al. 2004). For instance, lacO arrays inserted near budding yeast ce...

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“…We therefore hypothesized that Set2 degradation might alter the levels of H3K36me2/me3 to facilitate transcription elongation during periods of transcriptional stress, when, for example, chromatin compaction by Rpd3(S) would inhibit rapid gene activation of stress response genes (47,48). To examine this possibility, by way of using mutant forms of Set2 that have different behaviors in degradation and H3K36me, we expressed the different truncated forms of Set2 (see Fig.…”

Section: Overexpression Of More Stable Form Of Set2(1-261) Is Lethal mentioning

confidence: 99%

RNA Polymerase II Carboxyl-terminal Domain Phosphorylation Regulates Protein Stability of the Set2 Methyltransferase and Histone H3 Di- and Trimethylation at Lysine 36

Fuchs

Kizer

Braberg

et al. 2012

Journal of Biological Chemistry

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Background: Set2 catalyzes mono-, di-, and trimethylation of lysine 36 on histone H3 (H3K36). Results: Phosphorylation of the C-terminal domain of RNA polymerase II (RNAPII CTD) regulates Set2 protein levels and H3K36 methylation. Conclusion: Set2 protein is regulated to maintain balanced levels of H3K36 methylation. Significance: These results suggest that different methylation states perform distinct biological functions.

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Stress-Dependent Dynamics of Global Chromatin Remodeling in Yeast: Dual Role for SWI/SNF in the Heat Shock Stress Response

Cited by 128 publications

References 61 publications

Chromatin and Transcription in Yeast

Chromatin and Transcription in Yeast

Targeted INO80 enhances subnuclear chromatin movement and ectopic homologous recombination

RNA Polymerase II Carboxyl-terminal Domain Phosphorylation Regulates Protein Stability of the Set2 Methyltransferase and Histone H3 Di- and Trimethylation at Lysine 36

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