ArticleMolecular biology of the cell2007
Expansion of chromosome territories with chromatin decompaction in BAF53-depleted interphase cells.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Phosphorylation of Drosophila Brahma on CDK-phosphorylation sites is important for cell cycle regulation and differentiation.Cell cycle (Georgetown, Tex.) · 2018Article
- Baf53a is involved in survival of mouse ES cells, which can be compensated by Baf53b.Scientific reports · 2017Article
- Heterozygous variants in ACTL6A, encoding a component of the BAF complex, are associated with intellectual disability.Human mutation · 2017Article
- The Actin-Related Protein BAF53 Is Essential for Chromosomal Subdomain Integrity.Molecules and cells · 2015Article
- Chromatin structure and replication origins: determinants of chromosome replication and nuclear organization.Journal of molecular biology · 2014Review
- Basic concepts of epigenetics: impact of environmental signals on gene expression.Epigenetics · 2012Review
- Varying modulation of HIV-1 LTR activity by Baf complexes.Journal of molecular biology · 2011Article
- Looping probabilities in model interphase chromosomes.Biophysical journal · 2010Article
- Actin complexes in the cell nucleus: new stones in an old field.Histochemistry and cell biology · 2010Review
- Actin-related protein Arp6 influences H2A.Z-dependent and -independent gene expression and links ribosomal protein genes to nuclear pores.PLoS genetics · 2010Article
- Histone H1 subtypes differentially modulate chromatin condensation without preventing ATP-dependent remodeling by SWI/SNF or NURF.PloS one · 2009Article
- The SWI/SNF complex and cancer.Oncogene · 2009Review
- Chapter 5. Nuclear actin-related proteins in epigenetic control.International review of cell and molecular biology · 2009Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chromosomes are compartmentalized into discrete chromosome territories during interphase in mammalian cells. A chromosome territory is generated by the tendency of chromatin to occupy the smallest shell volume, which is determined by the polymeric properties and interactions of the internal meshwork of the chromatin fiber. Here, we show that BAF53 knockdown by small interfering RNA interference led to the expansion of chromosome territories. This was accompanied by a reduction in chromatin compaction, an increase in the micrococcal nuclease sensitivity of the chromatin, and an alteration in H3-K9 and H3-K79 dimethylation. Interestingly, the BAF53 knockdown cells suffer a cell cycle defect. Despite the significant irregularity and decompaction of the polynucleosomes isolated from the BAF53 knockdown cells, the chromatin loading of H1 and core histones remained unaltered, as did the nucleosome spacing. The histone hyperacetylation and down-regulation of BRG-1, mBrm, and Tip49, the catalytic components of the SWI/SNF complex and the TIP60 complex, respectively, did not expand chromosome territories. These results indicate that BAF53 contributes to the polymeric properties and/or the internal meshwork interactions of the chromatin fiber probably via a novel mechanism.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.