Details

Autor(en) / Beteiligte

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

Titel

Ectopic histone H3S10 phosphorylation causes chromatin structure remodeling in Drosophila

Ist Teil von

• Development (Cambridge), 2008-02, Vol.135 (4), p.699-705

Ort / Verlag

England: The Company of Biologists Limited

Erscheinungsjahr

2008

Quelle

MEDLINE

Beschreibungen/Notizen

• 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.