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Histone variant H2A.Z regulates centromere silencing and chromosome segregation in fission yeast

Academic Article
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Overview

authors

  • Hou, H. T.
  • Wang, Y.
  • Kallgren, S. P.
  • Thompson, J.
  • Yates III, John
  • Jia, S. T.

publication date

  • January 2010

journal

  • Journal of Biological Chemistry  Journal

abstract

  • The incorporation of histone variant H2A.Z into nucleosomes plays essential roles in regulating chromatin structure and gene expression. A multisubunit complex containing chromatin remodeling protein Swr1 is responsible for the deposition of H2A.Z in budding yeast and mammals. Here, we show that the JmjC domain protein Msc1 is a novel component of the fission yeast Swr1 complex and is required for Swr1-mediated incorporation of H2A.Z into nucleosomes at gene promoters. Loss of Msc1, Swr1, or H2A.Z results in loss of silencing at centromeres and defective chromosome segregation, although centromeric levels of CENP-A, a centromere-specific histone H3 variant that is required for setting up the chromatin structure at centromeres, remain unchanged. Intriguingly, H2A.Z is required for the expression of another centromere protein, CENP-C, and overexpression of CENP-C rescues centromere silencing defects associated with H2A.Z loss. These results demonstrate the importance of H2A.Z and CENP-C in maintaining a silenced chromatin state at centromeres.

subject areas

  • Adenosine Triphosphatases
  • Amino Acid Sequence
  • Animals
  • Centromere
  • Chromatin
  • Chromosomal Proteins, Non-Histone
  • Chromosome Segregation
  • DNA-Binding Proteins
  • Gene Silencing
  • Histones
  • Homeodomain Proteins
  • Humans
  • Molecular Sequence Data
  • Mutation
  • Promoter Regions, Genetic
  • Saccharomyces cerevisiae Proteins
  • Schizosaccharomyces
  • Schizosaccharomyces pombe Proteins
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Identity

PubMed Central ID

  • PMC2804349

International Standard Serial Number (ISSN)

  • 0021-9258

Digital Object Identifier (DOI)

  • 10.1074/jbc.M109.058487

PubMed ID

  • 19910462
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Additional Document Info

start page

  • 1909

end page

  • 1918

volume

  • 285

issue

  • 3

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