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First published online November 24, 2004


Journal of Cell Science 117, 2503e (2004)
© The Company of Biologists Limited
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In this issue

Heterochromatin awakes


As cells differentiate, much of their DNA is silenced, forming blocks of `facultative' heterochromatin. This has characteristic epigenetic features (e.g. specific histone modifications) and differs from the `constitutive' heterochromatin of gene-poor regions such as centromeres. To gain insight into how heterochromatin is reorganized during cell differentiation and reactivation, Christopher Woodcock and coworkers have tracked the epigenetic changes that occur during reactivation of quiescent T cells by mitogens (see p. 6153). Their findings reveal that it is much more dynamic than previously thought. They show that the heterochromatin-associated proteins HP1 and macroH2A (a histone variant) dramatically redistribute during T cell reactivation: macro2HA is lost from pericentromeric chromatin whereas HP1{alpha} moves into it. Significantly, the reverse occurs when they induce fibroblasts to become quiescent. This indicates that reciprocal exchange of these proteins might underpin a general mechanism for heterochromatin remodelling. Perhaps the authors' most interesting discovery, however, is a novel nuclear domain around centromeres that contains histones with modifications characteristic of heterochromatin (e.g dimethylation of Lys9 of histone H3). This `apocentric zone' is evident in quiescent cells and might represent a specific nuclear environment whose activity is influenced by the centromeric heterochromatin.


Related articles in JCS:

Dynamic relocation of epigenetic chromatin markers reveals an active role of constitutive heterochromatin in the transition from proliferation to quiescence
Sergei A. Grigoryev, Tatiana Nikitina, John R. Pehrson, Prim B. Singh, and Christopher L. Woodcock
JCS 2004 117: 6153-6162. [Abstract] [Full Text]  




This Article
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