ATP-Driven Exchange of Histone H2AZ Variant Catalyzed by SWR1 Chromatin Remodeling Complex

  • Gaku Mizuguchi
    Laboratory of Molecular Cell Biology, National Cancer Institute, National Institutes of Health, Building 37, Room 6068, Bethesda, MD 20892–4255, USA.
  • Xuetong Shen
    Laboratory of Molecular Cell Biology, National Cancer Institute, National Institutes of Health, Building 37, Room 6068, Bethesda, MD 20892–4255, USA.
  • Joe Landry
    Laboratory of Molecular Cell Biology, National Cancer Institute, National Institutes of Health, Building 37, Room 6068, Bethesda, MD 20892–4255, USA.
  • Wei-Hua Wu
    Laboratory of Molecular Cell Biology, National Cancer Institute, National Institutes of Health, Building 37, Room 6068, Bethesda, MD 20892–4255, USA.
  • Subhojit Sen
    Laboratory of Molecular Cell Biology, National Cancer Institute, National Institutes of Health, Building 37, Room 6068, Bethesda, MD 20892–4255, USA.
  • Carl Wu
    Laboratory of Molecular Cell Biology, National Cancer Institute, National Institutes of Health, Building 37, Room 6068, Bethesda, MD 20892–4255, USA.

抄録

<jats:p>The conserved histone variant H2AZ has an important role in the regulation of gene expression and the establishment of a buffer to the spread of silent heterochromatin. How histone variants such as H2AZ are incorporated into nucleosomes has been obscure. We have found that Swr1, a Swi2/Snf2-related adenosine triphosphatase, is the catalytic core of a multisubunit, histone-variant exchanger that efficiently replaces conventional histone H2A with histone H2AZ in nucleosome arrays. Swr1 is required for the deposition of histone H2AZ at specific chromosome locations in vivo, and Swr1 and H2AZ commonly regulate a subset of yeast genes. These findings define a previously unknown role for the adenosine triphosphate–dependent chromatin remodeling machinery.</jats:p>

収録刊行物

  • Science

    Science 303 (5656), 343-348, 2004-01-16

    American Association for the Advancement of Science (AAAS)

被引用文献 (43)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ