Variations in the composition of mammalian SWI/SNF chromatin remodelling complexes

Ryme, Jessica; Asp, Patrik; Böhm, Stefanie; Cavellán, Erica; Farrants, Ann Kristin Östlund

doi:10.1002/jcb.22288

Cited by 41 publications

(44 citation statements)

References 53 publications

(106 reference statements)

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“…Histologically, hearts of BAF180 knockout mice exhibit ventricular wall thinning with ventricular septal defect [61]. Interestingly, the atrioventricular valves and neural crest-derived aortic and pulmonary artery outflow tracts and their valves are unperturbed [62,63]. Notably, the phenotype observed in BAF180-deficient mice is very similar to the phenotype of RxRa knockout (KO) mice.…”

Section: Role Of Chromatin-modifying Enzymes In Cardiac Developmentmentioning

confidence: 52%

Epigenetic mechanisms in cardiac development and disease

Vallaster¹,

Vallaster²,

Wu³

2012

ABBS

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During mammalian development, cardiac specification and ultimately lineage commitment to a specific cardiac cell type is accomplished by the action of specific transcription factors (TFs) and their meticulous control on an epigenetic level. In this review, we detail how cardiacspecific TFs function in concert with nucleosome remodeling and histone-modifying enzymes to regulate a diverse network of genes required for processes such as cell growth and proliferation, or epithelial to mesenchymal transition (EMT), for instance. We provide examples of how several cardiac TFs, such as Nkx2.5, WHSC1, Tbx5, and Tbx1, which are associated with developmental and congenital heart defects, are required for the recruitment of histone modifiers, such as Jarid2, p300, and Ash2l, and components of ATP-dependent remodeling enzymes like Brg1, Baf60c, and Baf180. Binding of these TFs to their respective sites at cardiac genes coincides with a distinct pattern of histone marks, indicating that the precise regulation of cardiac gene networks is orchestrated by interactions between TFs and epigenetic modifiers. Furthermore, we speculate that an epigenetic signature, comprised of TF occupancy, histone modifications, and overall chromatin organization, is an underlying mechanism that governs cardiac morphogenesis and disease.

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Section: Role Of Chromatin-modifying Enzymes In Cardiac Developmentmentioning

confidence: 52%

Epigenetic mechanisms in cardiac development and disease

Vallaster¹,

Vallaster²,

Wu³

2012

ABBS

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“…In addition, targeting of individual subunits to synthetic reporter genes confirms diverse subunit function in transcriptional regulation (57). These observations have important implications for gene expression, since varied compositions of the SWI/SNF, ISW1, and SWR1 complexes at specific target genes have been linked to varied rates of transcription (40,(60)(61)(62). Moreover, subcellular localization of chromatinremodeling subunits can change in response to stress, further indicating the adaptable functionality of chromatin remodelers in coordination with environmental conditions (63).…”

Section: Discussionmentioning

confidence: 81%

The INO80 Complex Requires the Arp5-Ies6 Subcomplex for Chromatin Remodeling and Metabolic Regulation

Yao

King

Beckwith

et al. 2016

Molecular and Cellular Biology

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d ATP-dependent chromatin remodeling complexes are essential for transcription regulation, and yet it is unclear how these multisubunit complexes coordinate their activities to facilitate diverse transcriptional responses. In this study, we found that the conserved Arp5 and Ies6 subunits of the Saccharomyces cerevisiae INO80 chromatin-remodeler form an abundant and distinct subcomplex in vivo and stimulate INO80-mediated activity in vitro. Moreover, our genomic studies reveal that the relative occupancy of Arp5-Ies6 correlates with nucleosome positioning at transcriptional start sites and expression levels of >1,000 INO80-regulated genes. Notably, these genes are significantly enriched in energy metabolism pathways. Specifically, arp5⌬, ies6⌬, and ino80⌬ mutants demonstrate decreased expression of genes involved in glycolysis and increased expression of genes in the oxidative phosphorylation pathway. Deregulation of these metabolic pathways results in constitutively elevated mitochondrial potential and oxygen consumption. Our results illustrate the dynamic nature of the INO80 complex assembly and demonstrate for the first time that a chromatin remodeler regulates glycolytic and respiratory capacity, thereby maintaining metabolic stability. E ukaryotic genomic DNA is assembled with histones to form chromatin, a complex structure that undergoes constant dynamic reorganization in coordination with DNA-templated processes. Chromatin remodeling, an ATP-dependent mechanism by which nucleosomes are repositioned and reconstructed, is a fundamental component of chromatin manipulation and influences numerous DNA-templated pathways. Because chromatin remodelers are involved in essential cellular processes, defects in remodeling activity directly result in fitness deficiencies in lower eukaryotes, as well as developmental defects and disease in higher eukaryotes (1, 2).In particular, disruption of INO80, an evolutionarily conserved chromatin remodeling complex, results in pluripotency defects and carcinogenesis (3-6). The INO80 complex has demonstrated roles in transcription (7-9), replication (10-12), DNA damage responses (13-16), telomere regulation (17), and mitotic stability (18,19). These studies exemplify the functional diversity of the INO80 complex in different pathways (20). Moreover, they highlight the need for regulatory mechanisms that direct its activity among, and within, these processes.Ample opportunities for regulation of chromatin remodeling exist at the level of individual remodeler complex subunits. For example, different subunits of the INO80 complex are involved in DNA repair and cell cycle checkpoint responses (13, 16). Structural studies demonstrate that these subunits are components of different modules that interact with distinct domains of the S. cerevisiae Ino80 ATPase subunit (21) and thus may impart regulatory functions on ATP-dependent activities of the INO80 complex.For example, a module consisting of actin and actin-related proteins (Arps) Arp8 and Arp4 interacts with the helicase-associated...

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“…2). Common gene targets have been noted before, both cooperative and antagonistic (44), with a suggestion that hybrid complexes are capable of forming on individual promoters (48). Nevertheless, the lack of requirement for ARID2 in maintaining early repression of the late-stage markers Dmp1 and Phex clearly distinguishes the role of ARID2-containing complexes from the totality of BRG1 functions.…”

Section: Discussionmentioning

confidence: 86%

Essential Role of ARID2 Protein-containing SWI/SNF Complex in Tissue-specific Gene Expression

Flowers

Morán

2012

Journal of Biological Chemistry

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Background:The ARID2 protein is specific for a certain subset of SWI/SNF chromatin-remodeling complexes known as PBAF. Results: ARID2 is essential for gene activation along the osteoblast phenotype. Conclusion: ARID2-containing complexes play a major role in lineage commitment and differentiation. Significance: Manipulating levels of ARID family subunits (of which there are three mutually exclusive alternatives in SWI/ SNF) may influence precursor state and lineage determination without compromising full SWI/SNF function.

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Variations in the composition of mammalian SWI/SNF chromatin remodelling complexes

Cited by 41 publications

References 53 publications

Epigenetic mechanisms in cardiac development and disease

Epigenetic mechanisms in cardiac development and disease

The INO80 Complex Requires the Arp5-Ies6 Subcomplex for Chromatin Remodeling and Metabolic Regulation

Essential Role of ARID2 Protein-containing SWI/SNF Complex in Tissue-specific Gene Expression

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