Ectopic histone H3S10 phosphorylation causes chromatin structure remodeling in Drosophila
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.
This article is published as Deng, Huai, Xiaomin Bao, Weili Cai, Melissa J. Blacketer, Andrew S. Belmont, Jack Girton, Jørgen Johansen, and Kristen M. Johansen. "Ectopic histone H3S10 phosphorylation causes chromatin structure remodeling in Drosophila." Development 135, no. 4 (2008): 699-705. doi: 10.1242/dev.015362.