The SWI/SNF complex acts to constrain distribution of the centromeric histone variant Cse4. Gkikopoulos, T., Singh, V., Tsui, K., Awad, S., Renshaw, M. J., Scholfield, P., Barton, G. J., Nislow, C., Tanaka, T. U., & Owen-Hughes, T. The EMBO journal, 30(10):1919--1927, May, 2011.
doi  abstract   bibtex   
In order to gain insight into the function of the Saccharomyces cerevisiae SWI/SNF complex, we have identified DNA sequences to which it is bound genomewide. One surprising observation is that the complex is enriched at the centromeres of each chromosome. Deletion of the gene encoding the Snf2 subunit of the complex was found to cause partial redistribution of the centromeric histone variant Cse4 to sites on chromosome arms. Cultures of snf2Δ yeast were found to progress through mitosis slowly. This was dependent on the mitotic checkpoint protein Mad2. In the absence of Mad2, defects in chromosome segregation were observed. In the absence of Snf2, chromatin organisation at centromeres is less distinct. In particular, hypersensitive sites flanking the Cse4 containing nucleosomes are less pronounced. Furthermore, SWI/SNF complex was found to be especially effective in the dissociation of Cse4 containing chromatin in vitro. This suggests a role for Snf2 in the maintenance of point centromeres involving the removal of Cse4 from ectopic sites.
@article{ gkikopoulos_swi/snf_2011,
  title = {The {SWI}/{SNF} complex acts to constrain distribution of the centromeric histone variant {Cse}4},
  volume = {30},
  issn = {1460-2075},
  doi = {10.1038/emboj.2011.112},
  abstract = {In order to gain insight into the function of the Saccharomyces cerevisiae SWI/SNF complex, we have identified DNA sequences to which it is bound genomewide. One surprising observation is that the complex is enriched at the centromeres of each chromosome. Deletion of the gene encoding the Snf2 subunit of the complex was found to cause partial redistribution of the centromeric histone variant Cse4 to sites on chromosome arms. Cultures of snf2Δ yeast were found to progress through mitosis slowly. This was dependent on the mitotic checkpoint protein Mad2. In the absence of Mad2, defects in chromosome segregation were observed. In the absence of Snf2, chromatin organisation at centromeres is less distinct. In particular, hypersensitive sites flanking the Cse4 containing nucleosomes are less pronounced. Furthermore, SWI/SNF complex was found to be especially effective in the dissociation of Cse4 containing chromatin in vitro. This suggests a role for Snf2 in the maintenance of point centromeres involving the removal of Cse4 from ectopic sites.},
  language = {eng},
  number = {10},
  journal = {The EMBO journal},
  author = {Gkikopoulos, Triantaffyllos and Singh, Vijender and Tsui, Kyle and Awad, Salma and Renshaw, Matthew J. and Scholfield, Pieta and Barton, Geoffrey J. and Nislow, Corey and Tanaka, Tomoyuki U. and Owen-Hughes, Tom},
  month = {May},
  year = {2011},
  pmid = {21505420},
  pmcid = {PMC3098484},
  keywords = {Adenosine Triphosphatases, Binding Sites, Centromere, Chromatin Assembly and Disassembly, Chromosomal Proteins, Non-Histone, Chromosome Segregation, DAG, DNA, Fungal, DNA-Binding Proteins, Gene Deletion, Protein Binding, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Transcription Factors},
  pages = {1919--1927}
}

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