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TNFα signals through specialized factories where responsive coding and miRNA genes are transcribed

Identifieur interne : 000B73 ( Istex/Curation ); précédent : 000B72; suivant : 000B74

TNFα signals through specialized factories where responsive coding and miRNA genes are transcribed

Auteurs : Argyris Papantonis [Royaume-Uni] ; Takahide Kohro [Japon] ; Sabyasachi Baboo [Royaume-Uni] ; Joshua D. Larkin [Royaume-Uni] ; Binwei Deng [Royaume-Uni] ; Patrick Short [Royaume-Uni, États-Unis] ; Shuichi Tsutsumi [Japon] ; Stephen Taylor [Royaume-Uni] ; Yasuharu Kanki [Japon] ; Mika Kobayashi [Japon] ; Guoliang Li [Singapour] ; Huay-Mei Poh [Singapour] ; Xiaoan Ruan [Singapour] ; Hiroyuki Aburatani [Japon] ; Yijun Ruan [Singapour] ; Tatsuhiko Kodama [Japon] ; Youichiro Wada [Japon] ; Peter R. Cook [Royaume-Uni]

Source :

RBID : ISTEX:8E1FF2C72C55B5D7D0DE8893B791392AC098BFB2

English descriptors

Abstract

Tumour necrosis factor alpha (TNFα) is a potent cytokine that signals through nuclear factor kappa B (NFκB) to activate a subset of human genes. It is usually assumed that this involves RNA polymerases transcribing responsive genes wherever they might be in the nucleus. Using primary human endothelial cells, variants of chromosome conformation capture (including 4C and chromatin interaction analysis with paired‐end tag sequencing), and fluorescence in situ hybridization to detect single nascent transcripts, we show that TNFα induces responsive genes to congregate in discrete ‘NFκB factories’. Some factories further specialize in transcribing responsive genes encoding micro‐RNAs that target downregulated mRNAs. We expect all signalling pathways to contain this extra leg, where responding genes are transcribed in analogous specialized factories.
TNFα alpha treatment induces congregation of both coding and non‐coding NFκB target genes in discrete transcription factories, leading to coordinated gene expression.

Url:
DOI: 10.1038/emboj.2012.288

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ISTEX:8E1FF2C72C55B5D7D0DE8893B791392AC098BFB2

Le document en format XML

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<name sortKey="Kobayashi, Mika" sort="Kobayashi, Mika" uniqKey="Kobayashi M" first="Mika" last="Kobayashi">Mika Kobayashi</name>
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<mods:affiliation>Department of Applied Mathematics and Quantitative Biology, University of North Carolina, NC, Chapel Hill, USA</mods:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Applied Mathematics and Quantitative Biology, University of North Carolina, NC, Chapel Hill</wicri:regionArea>
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<name sortKey="Tsutsumi, Shuichi" sort="Tsutsumi, Shuichi" uniqKey="Tsutsumi S" first="Shuichi" last="Tsutsumi">Shuichi Tsutsumi</name>
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<name sortKey="Taylor, Stephen" sort="Taylor, Stephen" uniqKey="Taylor S" first="Stephen" last="Taylor">Stephen Taylor</name>
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<name sortKey="Kanki, Yasuharu" sort="Kanki, Yasuharu" uniqKey="Kanki Y" first="Yasuharu" last="Kanki">Yasuharu Kanki</name>
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<name sortKey="Kobayashi, Mika" sort="Kobayashi, Mika" uniqKey="Kobayashi M" first="Mika" last="Kobayashi">Mika Kobayashi</name>
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<name sortKey="Aburatani, Hiroyuki" sort="Aburatani, Hiroyuki" uniqKey="Aburatani H" first="Hiroyuki" last="Aburatani">Hiroyuki Aburatani</name>
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<name sortKey="Ruan, Yijun" sort="Ruan, Yijun" uniqKey="Ruan Y" first="Yijun" last="Ruan">Yijun Ruan</name>
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<name sortKey="Kodama, Tatsuhiko" sort="Kodama, Tatsuhiko" uniqKey="Kodama T" first="Tatsuhiko" last="Kodama">Tatsuhiko Kodama</name>
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<title level="j" type="main">The EMBO Journal</title>
<title level="j" type="alt">THE EMBO JOURNAL</title>
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<term>Active genes</term>
<term>Binding sites</term>
<term>Biol</term>
<term>Biology organization</term>
<term>Cell biol</term>
<term>Chromatin</term>
<term>Chromatin interaction analysis</term>
<term>Chromosome</term>
<term>Chromosome conformation</term>
<term>Colocalization</term>
<term>Colocalize</term>
<term>Conformation</term>
<term>Conventional sequencing</term>
<term>Cytokine</term>
<term>Different chromosomes</term>
<term>Different genes</term>
<term>Embo</term>
<term>Embo journal</term>
<term>Encoding</term>
<term>England biolabs</term>
<term>Ets2</term>
<term>Exact test</term>
<term>Ext1</term>
<term>Ezna microelute</term>
<term>Fewer contacts</term>
<term>Frequent contacts</term>
<term>Gene</term>
<term>Genes encoding mirnas</term>
<term>Genet</term>
<term>Genic</term>
<term>Genic contacts</term>
<term>Genome</term>
<term>Green foci</term>
<term>Hindiii</term>
<term>Human genes</term>
<term>Human genome</term>
<term>Huvecs</term>
<term>Intron</term>
<term>Intronic</term>
<term>Intronic probes</term>
<term>Koinuma</term>
<term>Microarray</term>
<term>Mirna</term>
<term>Mirna genes</term>
<term>Mirnas</term>
<term>More contacts</term>
<term>Mrna</term>
<term>Mrna levels</term>
<term>Multiplexed</term>
<term>Nascent</term>
<term>Nascent rnas</term>
<term>Nascent transcripts</term>
<term>Nfkb</term>
<term>Nuclear factor kappa</term>
<term>Other genes</term>
<term>Papantonis</term>
<term>Phosphorylation</term>
<term>Polymerase</term>
<term>Promoter</term>
<term>Rank order</term>
<term>Reference genes</term>
<term>Reference points</term>
<term>Responsive</term>
<term>Responsive gene</term>
<term>Responsive genes</term>
<term>Responsive promoters</term>
<term>Rna</term>
<term>Samd4a</term>
<term>Samd4a intron</term>
<term>Samd4a libraries</term>
<term>Same strategy</term>
<term>Sequencing</term>
<term>Specialized factories</term>
<term>Specialized transcription factories</term>
<term>Subunit</term>
<term>Supplementary</term>
<term>Supplementary figure</term>
<term>Supplementary figures</term>
<term>Supplementary table</term>
<term>Supplementary tables</term>
<term>Tgfb</term>
<term>Tnfa</term>
<term>Tnfa stimulation</term>
<term>Transcribing</term>
<term>Transcription</term>
<term>Transcription factories</term>
<term>Upregulated</term>
<term>Upregulated genes</term>
<term>Wada</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract">Tumour necrosis factor alpha (TNFα) is a potent cytokine that signals through nuclear factor kappa B (NFκB) to activate a subset of human genes. It is usually assumed that this involves RNA polymerases transcribing responsive genes wherever they might be in the nucleus. Using primary human endothelial cells, variants of chromosome conformation capture (including 4C and chromatin interaction analysis with paired‐end tag sequencing), and fluorescence in situ hybridization to detect single nascent transcripts, we show that TNFα induces responsive genes to congregate in discrete ‘NFκB factories’. Some factories further specialize in transcribing responsive genes encoding micro‐RNAs that target downregulated mRNAs. We expect all signalling pathways to contain this extra leg, where responding genes are transcribed in analogous specialized factories.</div>
<div type="abstract">TNFα alpha treatment induces congregation of both coding and non‐coding NFκB target genes in discrete transcription factories, leading to coordinated gene expression.</div>
</front>
</TEI>
</record>

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