Ectopic histone H3S10 phosphorylation causes chromatin structure remodeling in Drosophila

Huai Deng, Xiaomin Bao, Weili Cai, Melissa J. Blacketer, Andrew S. Belmont, Jack Girton, Jørgen Johansen, Kristen M. Johansen*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

48 Scopus citations

Abstract

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 Lac1-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' Lacl-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.

Original languageEnglish (US)
Pages (from-to)699-705
Number of pages7
JournalDevelopment
Volume135
Issue number4
DOIs
StatePublished - Feb 2008

Keywords

  • Chromatin structure remodeling
  • Drosophila
  • Histone H3S10 phosphorylation
  • JIL-1 kinase

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology

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