Ectopic histone H3S10 phosphorylation causes chromatin structure remodeling in Drosophila

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dc.contributor.author Deng, Huai
dc.contributor.author Bao, Xiaomin
dc.contributor.author Johansen, Kristen
dc.contributor.author Cai, Weili
dc.contributor.author Blacketer, Melissa
dc.contributor.author Belmont, Andrew
dc.contributor.author Girton, Jack
dc.contributor.author Johansen, Jorgen
dc.contributor.author Johansen, Kristen
dc.contributor.department Biochemistry, Biophysics and Molecular Biology
dc.date 2019-09-12T20:37:56.000
dc.date.accessioned 2020-06-29T23:46:40Z
dc.date.available 2020-06-29T23:46:40Z
dc.date.copyright Tue Jan 01 00:00:00 UTC 2008
dc.date.issued 2008-01-01
dc.description.abstract <p>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 <em>Drosophila</em> 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 <em>Drosophila</em> in vivo.</p>
dc.description.comments <p>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." <em>Development</em> 135, no. 4 (2008): 699-705. doi: <a href="https://doi.org/10.1242/dev.015362" target="_blank">10.1242/dev.015362</a>.</p>
dc.format.mimetype application/pdf
dc.identifier archive/lib.dr.iastate.edu/bbmb_ag_pubs/235/
dc.identifier.articleid 1238
dc.identifier.contextkey 14574529
dc.identifier.s3bucket isulib-bepress-aws-west
dc.identifier.submissionpath bbmb_ag_pubs/235
dc.identifier.uri https://dr.lib.iastate.edu/handle/20.500.12876/10705
dc.language.iso en
dc.source.bitstream archive/lib.dr.iastate.edu/bbmb_ag_pubs/235/2008_Johansen_EctopicHistone.pdf|||Fri Jan 14 22:48:51 UTC 2022
dc.source.uri 10.1242/dev.015362
dc.subject.disciplines Biochemistry, Biophysics, and Structural Biology
dc.subject.disciplines Cell and Developmental Biology
dc.subject.disciplines Genetics
dc.subject.disciplines Molecular Biology
dc.subject.disciplines Molecular Genetics
dc.subject.keywords Histone H3S10 phosphorylation
dc.subject.keywords Chromatin structure remodeling
dc.subject.keywords JIL-1 kinase
dc.subject.keywords Drosophila
dc.title Ectopic histone H3S10 phosphorylation causes chromatin structure remodeling in Drosophila
dc.type article
dc.type.genre article
dspace.entity.type Publication
relation.isAuthorOfPublication 3829d759-f8ec-4502-a63a-1655d3b70ef5
relation.isOrgUnitOfPublication c70f85ae-e0cd-4dce-96b5-4388aac08b3f
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