Mammalian SWI/SNF complexes promote MyoD-mediated muscle differentiation

Serna, Ivana L. de la; Carlson, Kerri A.; Imbalzano, Anthony N.

doi:10.1038/84826

Cited by 303 publications

(316 citation statements)

References 30 publications

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“…The role of SWI/SNF by all indications is far reaching. In mammals it is involved in many developmental programs such as muscle [19][20][21][22], heart [23], blood [24], skeletal [25], neuron [26][27][28][29], adipocyte [30], liver [31] and immune system/Tcell development [32,33]. Yeast SWI/SNF has been shown to be involved in an early step in homologous recombination (HR) while RSC promotes HR at the stage of strand invasion [34,35].…”

Section: Nucleosome Remodeling Complexes Swi/snf Familymentioning

confidence: 99%

Mechanisms of ATP dependent chromatin remodeling

Gangaraju

Bartholomew

2007

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

128

159

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The inter-relationship between DNA repair and ATP dependent chromatin remodeling has begun to become very apparent with recent discoveries. ATP dependent remodeling complexes mobilize nucleosomes along DNA, promote the exchange of histones, or completely displace nucleosomes from DNA. These remodeling complexes are often categorized based on the domain organization of their catalytic subunit. The biochemical properties and structural information of several of these remodeling complexes are reviewed. The different models for how these complexes are able to mobilize nucleosomes and alter nucleosome structure are presented incorporating several recent findings. Finally the role of histone tails and their respective modifications in ATP-dependent remodeling are discussed.

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Section: Nucleosome Remodeling Complexes Swi/snf Familymentioning

confidence: 99%

Mechanisms of ATP dependent chromatin remodeling

Gangaraju

Bartholomew

2007

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

128

159

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“…Yellow fluorescent protein (YFP)-BRG1 and YFP-BRG1-K-R were generated by cloning of wild-type BRG1 and mutant BRG1-K-R into pEYFP-C2 and pEGFP-C2 vectors (Clontech, Palo Alto, CA). GFP-BRM and GFP BRG1 have been previously described (Reyes et al, 1997;de la Serna et al, 2001) and was provided by Christian Muchardt, (Institute Pasteur, Paris, France). The full-length MMTV-LTR driving transcription of the luciferase gene, pRSV-GR (glucocorticoid receptor) and pCMV ␤-Galactosidase (internal control) has been described previously (Lefebvre et al, 1991;Fragoso et al, 1998).…”

Section: Expression Vectorsmentioning

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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“…Further proof comes from gene knockout studies that show the impact of chromatin modifying activities on developmental decisions. There are many examples, including the role of chromatin remodeling activities such as Brg1 in myogenesis (de la Serna et al, 2001) and neurogenesis (Eroglu et al, 2006). Before being hoist upon my own petard, I accept that this does not in itself constitute proof-positive of epigenetics, but it is a very strong indicator.…”

Section: Do You Think That Many Developmental Decisions Are Epigenetimentioning

confidence: 98%

Epigenetics in development

Kiefer

2007

Developmental Dynamics

237

144

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It has become increasingly evident in recent years that development is under epigenetic control. Epigenetics is the study of heritable changes in gene function that occur independently of alterations to primary DNA sequence. The best-studied epigenetic modifications are DNA methylation, and changes in chromatin structure by histone modifications, and histone exchange. An exciting, new chapter in the field is the finding that long-distance chromosomal interactions also modify gene expression. Epigenetic modifications are key regulators of important developmental events, including X-inactivation, genomic imprinting, patterning by Hox genes and neuronal development. This primer covers these aspects of epigenetics in brief, and features an interview with two epigenetic scientists. Developmental Dynamics 236: 1144 -1156, 2007.

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Mammalian SWI/SNF complexes promote MyoD-mediated muscle differentiation

Cited by 303 publications

References 30 publications

Mechanisms of ATP dependent chromatin remodeling

Mechanisms of ATP dependent chromatin remodeling

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

Epigenetics in development

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