ATP-Dependent Chromatin-Remodeling Complexes

Vignali, Marissa; Hassan, Ahmed H.E.; Neely, Kristen E.; Workman, Jerry L.

doi:10.1128/mcb.20.6.1899-1910.2000

Cited by 665 publications

(496 citation statements)

References 128 publications

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“…For example, overexpression of Cyclin D1 has been shown to distinguish breast carcinomas and in situ breast lesions from benign lesions (WeinstatSaslow et al, 1995). Amongst other cDNAs up-regulated in the malignant cell library, were those corresponding to mRNAs for a putative G-protein-coupled receptor (Libert et al, 1989), for proteins associated with the mitotic spindle checkpoint, BUB3 (Brady and Hardwick, 2000) and with chromatin remodelling (Wang et al, 1996;Zhang et al, 1998;Vignali et al, 2000). Two cDNAs (LIM kinase and BUB3), which are differentially-expressed in the present malignant library, have also been found to be differentially expressed in a subtracted library representing cDNAs expressed in a pathologically homogeneous breast carcinoma specimen subtracted with cDNA from 50 000 ductal-carcinoma-in-situ cells microdissected from the surrounding normal tissue (Liu, 2001).…”

Section: Discussionmentioning

confidence: 99%

Identification of mRNAs differentially-expressed between benign and malignant breast tumour cells

et al. 2002

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Two suppression subtracted cDNA libraries have been constructed, one containing cDNAs to mRNAs present at a higher level in a benign human breast tumour-derived cell line relative to the malignant mammary cell line, MCF-7, and the other containing cDNAs present at a higher level in the MCF-7 cells relative to the benign cells. Randomly-picked cloned DNAs have been sequenced yielding 29 and 128 different cDNAs from the benign and malignant libraries, respectively. Using reverse Northern hybridisation, 76% and 83% of the cDNAs were differentially expressed by greater than two-fold, whilst 14% and 11% of cDNAs in the respective libraries were differentially expressed by more than 15-fold. Amongst these were oestrogenresponsive cDNAs and expressed sequence tags. One such oestrogen-responsive expressed sequence tag, M41, is transcribed from a gene located on chromosome 21q22.3, within an intron of a larger gene. The M41 gene contains oestrogen response elements, one of which is associated with alu repeats. M41 mRNA is expressed at a statistically significantly higher level in human breast cancer specimens than in normal human breast and benign lesions. In carcinomas, its up-regulation is associated with the development of the malignant cell.

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Section: Discussionmentioning

confidence: 99%

Identification of mRNAs differentially-expressed between benign and malignant breast tumour cells

et al. 2002

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“…ATP-dependent chromatin-remodeling complexes and histone-modifying complexes dynamically modulate chromatin structure both at the nucleosome as well as at a higher order level (Vignali et al, 2000;Jenuwein and Allis, 2001). We explored the consequences of ATPase-deficient remodeling proteins on chromatin structure by using a restriction enzyme accessibility assay to assess the disruption of local chromatin structure.…”

Section: Discussionmentioning

confidence: 99%

Chromatin Remodeling Complexes Interact Dynamically with a Glucocorticoid Receptor–regulated Promoter

Johnson

Elbi

Parekh

et al. 2008

MBoC

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Brahma (BRM) and Brahma-related gene 1 (BRG1) are the ATP-dependent catalytic subunits of the SWI/SNF family of chromatin-remodeling complexes. These complexes are involved in essential processes such as cell cycle, growth, differentiation, and cancer. Using imaging approaches in a cell line that harbors tandem repeats of stably integrated copies of the steroid responsive MMTV-LTR (mouse mammary tumor virus-long terminal repeat), we show that BRG1 and BRM are recruited to the MMTV promoter in a hormone-dependent manner. The recruitment of BRG1 and BRM resulted in chromatin remodeling and decondensation of the MMTV repeat as demonstrated by an increase in the restriction enzyme accessibility and in the size of DNA fluorescence in situ hybridization (FISH) signals. This chromatin remodeling event was concomitant with an increased occupancy of RNA polymerase II and transcriptional activation at the MMTV promoter. The expression of ATPase-deficient forms of BRG1 (BRG1-K-R) or BRM (BRM-K-R) inhibited the remodeling of local and higher order MMTV chromatin structure and resulted in the attenuation of transcription. In vivo photobleaching experiments provided direct evidence that BRG1, BRG1-K-R, and BRM chromatin-remodeling complexes have distinct kinetic properties on the MMTV array, and they dynamically associate with and dissociate from MMTV chromatin in a manner dependent on hormone and a functional ATPase domain. Our data provide a kinetic and mechanistic basis for the BRG1 and BRM chromatin-remodeling complexes in regulating gene expression at a steroid hormone inducible promoter. INTRODUCTIONThe eukaryotic genome is organized into higher order chromatin structures in the nucleus. The regulation of eukaryotic gene expression in the context of chromatin is a complex event and is essential for numerous cellular processes (Lemon and Tjian, 2000;Orphanides and Reinberg, 2002;Labrador and Corces, 2002;Maniatis and Reed, 2002;Felsenfeld and Groudine, 2003;Roberts and Orkin, 2004). Maintenance, establishment, and modification of global chromatin organization and local chromatin structure are modulated by a large number of chromatin-binding proteins that generate transcriptionally permissive or repressed chromatin domains in response to environmental stimuli (Workman and Kingston, 1998;Peterson and Workman, 2000;Jones and Kadonaga, 2000;Wu and Grunstein, 2000;Wolffe and Hansen, 2001;Becker et al., 2002). The association of linker histones and nonhistone and heterochromatin-specific proteins such as high mobility group proteins and HP1 play key roles in the generation of higher order chromatin structures (Arents et al., 1991; Luger et al., 1997;Bustin, 1999;Eissenberg and Elgin, 2000;Hill, 2001;Thomas and Travers, 2001;Woodcock and Dimitrov, 2001;Grewal and Elgin, 2002;Bianchi and Agresti, 2005;Bustin et al., 2005;Verschure et al., 2005). The stearically restricted environment presented by chromatin is in part overcome by multisubunit protein complexes that enzymatically regulate chromatin structure. These complexes can e...

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Section: Nih Public Accessmentioning

confidence: 99%

“…These modifications affect chromatin structure by altering histone-DNA or histone-histone contacts (25), and/or by collectively establishing a code that is recognized by downstream effector proteins and complexes (24). The chromatin-modifying activities are recruited to certain loci by sequencespecific transcription factors (26,27), or by association with RNA polymerase II (27,28).Since there are many proteins involved in modifying chromatin, our analysis emphasized mutants that were reported to affect the expression of HIS4 or to alter its chromatin structure. Mutations in RPD3, encoding an H4 histone deacetylase (26), were reported to reduce HIS4 expression about three-fold in one study (29), although no significant change was observed in another study (30).…”

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The histone methylase Set2p and the histone deacetylase Rpd3p repress meiotic recombination at the HIS4 meiotic recombination hotspot in Saccharomyces cerevisiae

et al. 2008

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The rate of meiotic recombination in the yeast Saccharomyces cerevisiae varies widely in different regions of the genome with some genes having very high levels of recombination (hotspots). A variety of experiments done in yeast suggest that hotspots are a feature of chromatin structure rather than a feature of primary DNA sequence. We examined the effects of mutating a variety of enzymes that affect chromatin structure on the recombination activity of the well-characterized HIS4 hotspot including the Set2p and Dot1p histone methylases, the Hda1p and Rpd3p histone deacetylases, the Sin4p global transcription regulator, and a deletion of one of the two copies of the genes encoding histone H3-H4. Loss of Set2p or Rpd3p substantially elevated HIS4 hotspot activity, and loss of Hda1p had a smaller stimulatory effect; none of the other alterations had a significant effect. The increase of HIS4 hotspot activity in set2 and rpd3 strains is likely to be related to the recent finding that histone H3 methylation by Set2p directs deacetylation of histones by Rpd3p. IntroductionThe rate of meiotic recombination varies considerably at different positions in the yeast genome (1,2). This variation reflects differences in the frequency of local meiosis-specific doublestrand DNA breaks (DSBs), the recombination-initiating lesion (3,4) catalyzed by Spo11p and associated proteins (5). There are several lines of evidence that the frequency of DSBs is regulated by elements of chromatin structure rather than primary DNA sequence (2). First, recombination hotspots exhibit hypersensitivity to nucleases (6-10). Some loci (8,9) undergo meiosis-specific alterations in nuclease sensitivity prior to DSB formation, although no such changes are observed at other loci (6). Since all nuclease-hypersensitive regions are not meiotic Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Conflicts of interest None. NIH Public AccessAuthor Manuscript DNA Repair (Amst) (6,10), "open" chromatin appears necessary, but not sufficient, for meiotic recombination hotspot activity. Second, insertion of a nucleosome-excluding sequence into the yeast genome creates a recombination hotspot (11). Third, the activity of some hotspots requires the binding of transcription factors, but not high levels of transcription (2). This result has been interpreted as indicating that chromatin modifications associated with transcription factor binding stimulate both transcription and recombination. Finally, some mutants that affect chromatin modifications reduce the frequency of meiosis-specific DSBs. In the yeast S. pombe, mutatio...

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ATP-Dependent Chromatin-Remodeling Complexes

Cited by 665 publications

References 128 publications

Identification of mRNAs differentially-expressed between benign and malignant breast tumour cells

Identification of mRNAs differentially-expressed between benign and malignant breast tumour cells

Chromatin Remodeling Complexes Interact Dynamically with a Glucocorticoid Receptor–regulated Promoter

The histone methylase Set2p and the histone deacetylase Rpd3p repress meiotic recombination at the HIS4 meiotic recombination hotspot in Saccharomyces cerevisiae

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