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First published online 16 January 2008
doi: 10.1242/dev.015362
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1 Department of Biochemistry, Biophysics, and Molecular Biology, Iowa State
University, Ames, IA 50011, USA.
2 Department of Cell and Structural Biology, University of Illinois, Urbana, IL
61801, USA.
* Author for correspondence (e-mail: kristen{at}iastate.edu)
Accepted 4 December 2007
Histones are subject to numerous post-translational modifications that correlate with the state of higher-order chromatin structure and gene expression. However, it is not clear whether changes in these epigenetic marks are causative regulatory factors in chromatin structure changes or whether they play a mainly reinforcing or maintenance role. In Drosophila phosphorylation of histone H3S10 in euchromatic chromatin regions by the JIL-1 tandem kinase has been implicated in counteracting heterochromatization and gene silencing. Here we show, using a LacI-tethering system, that JIL-1 mediated ectopic histone H3S10 phosphorylation is sufficient to induce a change in higher-order chromatin structure from a condensed heterochromatin-like state to a more open euchromatic state. This effect was absent when a `kinase dead' LacI-JIL-1 construct without histone H3S10 phosphorylation activity was expressed. Instead, the `kinase dead' construct had a dominant-negative effect, leading to a disruption of chromatin structure that was associated with a global repression of histone H3S10 phosphorylation levels. These findings provide direct evidence that the epigenetic histone tail modification of H3S10 phosphorylation at interphase can function as a causative regulator of higher-order chromatin structure in Drosophila in vivo.
Key words: Histone H3S10 phosphorylation, Chromatin structure remodeling, JIL-1 kinase, Drosophila
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