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Mediator links epigenetic silencing of neuronal gene expression with x-linked mental retardation
被引:197
作者:

Ding, Ning
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Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA
Univ Texas Hlth Sci Ctr San Antonio, Inst Biotechnol, San Antonio, TX 78245 USA Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA

Zhou, Haiying
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Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA
Univ Texas Hlth Sci Ctr San Antonio, Inst Biotechnol, San Antonio, TX 78245 USA Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA

Esteve, Pierre-Olivier
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机构:
New England Biolabs Inc, Ipswich, MA 01938 USA Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA

Chin, Hang Gyeong
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机构:
New England Biolabs Inc, Ipswich, MA 01938 USA Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA

Kim, Seokjoong
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Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA
Univ Texas Hlth Sci Ctr San Antonio, Inst Biotechnol, San Antonio, TX 78245 USA Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA

Xu, Xuan
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Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA
Univ Texas Hlth Sci Ctr San Antonio, Inst Biotechnol, San Antonio, TX 78245 USA Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA

Joseph, Sumy M.
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机构:
Greenwood Genet Ctr, Greenwood, SC 29646 USA Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA

Friez, Michael J.
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Greenwood Genet Ctr, Greenwood, SC 29646 USA Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA

Schwartz, Charles E.
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Greenwood Genet Ctr, Greenwood, SC 29646 USA Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA

Pradhan, Sriharsa
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h-index: 0
机构:
New England Biolabs Inc, Ipswich, MA 01938 USA Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA

Boyer, Thomas G.
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h-index: 0
机构:
Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA
Univ Texas Hlth Sci Ctr San Antonio, Inst Biotechnol, San Antonio, TX 78245 USA Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA
机构:
[1] Univ Texas Hlth Sci Ctr San Antonio, Dept Mol Med, San Antonio, TX 78245 USA
[2] Univ Texas Hlth Sci Ctr San Antonio, Inst Biotechnol, San Antonio, TX 78245 USA
[3] New England Biolabs Inc, Ipswich, MA 01938 USA
[4] Greenwood Genet Ctr, Greenwood, SC 29646 USA
关键词:
D O I:
10.1016/j.molcel.2008.05.023
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Mediator occupies a central role in RNA polymerase 11 transcription as a sensor, integrator, and processor of regulatory signals that converge on protein-coding gene promoters. Compared to its role in gene activation, little is known regarding the molecular mechanisms and biological implications of Mediator as a transducer of repressive signals. Here we describe a protein interaction network required for extraneuronal gene silencing comprising Mediator, G9a histone methyltransferase, and the RE1 silencing transcription factor (REST; also known as neuron restrictive silencer factor, NRSF). We show that the MED12 interface in Mediator links REST with G9a-dependent histone H3K9 dimethylation to suppress neuronal genes in nonneuronal cells. Notably, missense mutations in MED12 causing the X-linked mental retardation (XLMR) disorders FG syndrome and Lujan syndrome disrupt its REST corepressor function. These findings implicate Mediator in epigenetic restriction of neuronal gene expression to the nervous system and suggest a pathologic basis for MED12-associated XLMR involving impaired REST-dependent neuronal gene regulation.
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页码:347 / 359
页数:13
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