Chromatin Boundaries in Budding Yeast

Ishii, Kojiro; Arib, Ghislaine; Lin, Clayton; Houwe, Griet Van; Laemmli, Ulrich Karl

doi:10.1016/s0092-8674(02)00756-0

Cited by 339 publications

(317 citation statements)

References 49 publications

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“…However, a similar huge protein complex formed on the barrier, if not tethered on nuclear pore complex (NPC), does not have barrier activity. (51) These results support a topological mechanism of chromatin domain formation.…”

Section: Predictionssupporting

confidence: 56%

A hypothesis for chromatin domain opening

Liu

Ling

2003

BioEssays

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SummaryThe eukaryotic genome is organized into different domains by cis-acting elements, such as boundaries/ insulators and matrix attachment regions, and is packaged with different degrees of condensation. In the M phase, the chromatin becomes further highly condensed into chromosomes. The first step for transcriptional activation of a given gene, at a particular time during development, in any locus, is the opening of its chromatin domain. This locus needs to be kept in this state in each early G 1 phase during every cell cycle. Certain distal enhance elements, including locus control regions (LCRs) and enhancers, are believed to perform this target chromatin domain opening process and several models have been proposed to explain distal enhance action. But they did not explain precisely how a given chromatin domain is opened. Based on various studies, we propose a hypothesis for the mechanism of opening chromatin on a large scale. One important mechanism may involved breaking one or two DNA strands and reducing the linking numbers within chromatin domain. The topological changes can overpass some complexes formed on DNA strands and can be transmitted from specific localized points over a broad region, until boundary elements or insulators are reached. These may initiate downstream events such as propagation of histone acetylation and the binding of transcription factors to proximal promoters and may further augment the action mediated by distal enhancer elements.

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Section: Predictionssupporting

confidence: 56%

A hypothesis for chromatin domain opening

Liu

Ling

2003

BioEssays

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“…It has been suggested that chromatin loops are formed through association of insulator elements with the nuclear pores (32,33,52). It is therefore possible that the barrier elements flanking HMR (21,22) or the hypersensitive sites at this locus (45) associate with nuclear pores or active chromatin hubs and cluster in the nucleus, the consequence of which would be to align HMR-E and HMR-I in close proximity.…”

Section: Discussionmentioning

confidence: 99%

“…The ADE2 gene flanked by Gal4p binding sites (Gbs), present at HML, in strain KIY54 (32) was PCR amplified with appropriate primers and integrated at the HMR locus in a sir2⌬ strain (JRY4576) or in an HMR⌬I sir4⌬ strain (ROY926). Sequencing of the PCR products indicated that a single Gal4p binding site, which is contrary to published results (32), flanked ADE2.…”

Section: Methodsmentioning

confidence: 99%

“…It has been suggested that chromatin loops are formed by the attachment of barrier elements to the nuclear pore via Nup2p (32). Analyses of Nup2p mutants indicate that Nup2p is necessary for robust tRNA barrier function, but loss of Nup2p did not affect the long-range communication between the two silencers (G. Ruben and R. T. Kamakaka, unpublished data).…”

Section: Downloaded Frommentioning

confidence: 99%

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Long-Range Communication between the Silencers of HMR

Valenzuela

Dhillon

Dubey

et al. 2008

Molecular and Cellular Biology

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Gene regulation involves long-range communication between silencers, enhancers, and promoters. In Saccharomyces cerevisiae, silencers flank transcriptionally repressed genes to mediate regional silencing. Silencers recruit the Sir proteins, which then spread along chromatin to encompass the entire silenced domain. In this report we have employed a boundary trap assay, an enhancer activity assay, chromatin immunoprecipitations, and chromosome conformation capture analyses to demonstrate that the two HMR silencer elements are in close proximity and functionally communicate with one another in vivo. We further show that silencing is necessary for these long-range interactions, and we present models for Sir-mediated silencing based upon these results.Gene activation and gene repression are central to the proper development and differentiation of organisms. DNA elements such as promoters, enhancers, and silencers play a central role in eukaryotic gene regulation. These elements are separated from each other by several kilobase pairs of DNA but are able to communicate with one another to regulate the activation or repression of genes. The exact mechanism by which distally located elements communicate with one another is not clear and is one of the key questions in gene regulation. Long-range communication between distantly located elements in chromosomes is thought to occur by one of two principal mechanisms (8). One class of models postulate that a signal emanating from a distal regulatory element spreads along the DNA fiber until it encounters a proximal regulatory element. A second class of models postulate that distal and proximal regulatory elements interact with one another directly, with the intervening DNA forming a loop. Both mechanisms must function within the context of the global chromosome structure, which appears to be composed of large chromosome loops that attach to a proteinaceous superstructure (11). The nucleus appears to be divided further into distinct chromatin compartments, with heterochromatic domains being present in regions near the nuclear periphery while euchromatic domains are found mainly in the interior of the nucleus, although a significant portion of euchromatin is located near nuclear pores.It has been suggested that the functionally and structurally defined chromatin domains may be coincident (36). Enhancers and locus control regions (LCRs) are long-range regulatory elements that activate promoters in a distance-and orientation-independent manner, and recent studies indicate that enhancers and LCRs often cluster together in three-dimensional space to form an "active chromatin hub" (23,49,58,59).Similarly, in yeast the promoters and terminators of genes are in close proximity to one another (3, 48) and tethered to the nuclear pore (10, 52). The consequence of this spatial organization is that the DNA between these regulatory elements is looped out. It is thought that the formation of these nuclear substructures aids in transcription activation.Silencers are negative regulatory element...

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“…Although there is no evidence yet showing that specific pores bind specific sets of genes, recent studies implicate nuclear pores in a range of cellular processes, well beyond their function in macromolecular transport. Notably, in budding yeast and Drosophila certain highly transcribed, and in some cases stress-induced, genes are associated with nuclear pores [11][12][13][14][15][16][17][18][19]. This association not only promotes efficient export of mRNAs through coupling of transcription with export [10,11,13,14], but also helps modulate transcript levels of some loci.…”

Section: Introductionmentioning

confidence: 99%

Nuclear organization in genome stability: SUMO connections

2011

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Recent findings show that chromatin dynamics and nuclear organization are not only important for gene regulation and DNA replication, but also for the maintenance of genome stability. In yeast, nuclear pores play a role in the maintenance of genome stability by means of the evolutionarily conserved family of SUMO-targeted Ubiquitin ligases (STUbLs). The yeast Slx5/Slx8 STUbL associates with a class of DNA breaks that are shifted to nuclear pores. Functionally Slx5/Slx8 are needed for telomere maintenance by an unusual recombination-mediated pathway. The mammalian STUbL RNF4 associates with Promyelocytic leukaemia (PML) nuclear bodies and regulates PML/PMLfusion protein stability in response to arsenic-induced stress. A subclass of PML bodies support telomere maintenance by the ALT pathway in telomerase-deficient tumors. Perturbation of nuclear organization through either loss of pore subunits in yeast, or PML body perturbation in man, can lead to gene amplifications, deletions, translocations or endto-end telomere fusion events, thus implicating SUMO and STUbLs in the subnuclear organization of select repair events.

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Chromatin Boundaries in Budding Yeast

Cited by 339 publications

References 49 publications

A hypothesis for chromatin domain opening

A hypothesis for chromatin domain opening

Long-Range Communication between the Silencers of HMR

Nuclear organization in genome stability: SUMO connections

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