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MeCP2 Represses the Rate of Transcriptional Initiation of Highly Methylated Long Genes.
Molecular Cell ( IF 14.5 ) Pub Date : 2019-11-26 , DOI: 10.1016/j.molcel.2019.10.032 Lisa D Boxer 1 , William Renthal 1 , Alexander W Greben 1 , Tess Whitwam 1 , Andrew Silberfeld 1 , Hume Stroud 1 , Emmy Li 1 , Marty G Yang 1 , Benyam Kinde 1 , Eric C Griffith 1 , Boyan Bonev 2 , Michael E Greenberg 1
Molecular Cell ( IF 14.5 ) Pub Date : 2019-11-26 , DOI: 10.1016/j.molcel.2019.10.032 Lisa D Boxer 1 , William Renthal 1 , Alexander W Greben 1 , Tess Whitwam 1 , Andrew Silberfeld 1 , Hume Stroud 1 , Emmy Li 1 , Marty G Yang 1 , Benyam Kinde 1 , Eric C Griffith 1 , Boyan Bonev 2 , Michael E Greenberg 1
Affiliation
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Mutations in the methyl-DNA-binding repressor protein MeCP2 cause the devastating neurodevelopmental disorder Rett syndrome. It has been challenging to understand how MeCP2 regulates transcription because MeCP2 binds broadly across the genome and MeCP2 mutations are associated with widespread small-magnitude changes in neuronal gene expression. We demonstrate here that MeCP2 represses nascent RNA transcription of highly methylated long genes in the brain through its interaction with the NCoR co-repressor complex. By measuring the rates of transcriptional initiation and elongation directly in the brain, we find that MeCP2 has no measurable effect on transcriptional elongation, but instead represses the rate at which Pol II initiates transcription of highly methylated long genes. These findings suggest a new model of MeCP2 function in which MeCP2 binds broadly across highly methylated regions of DNA, but acts at transcription start sites to attenuate transcriptional initiation.
中文翻译：
MeCP2抑制高度甲基化的长基因的转录起始速率。
甲基-DNA结合阻遏蛋白MeCP2中的突变导致毁灭性神经发育障碍Rett综合征。理解MeCP2如何调节转录是一项挑战，因为MeCP2在整个基因组中广泛结合，并且MeCP2突变与神经元基因表达中普遍存在的小幅度变化有关。我们在这里证明MeCP2通过与NCoR协同阻遏物复合物的相互作用抑制大脑中高度甲基化的长基因的新生RNA转录。通过直接在大脑中测量转录起始和伸长的速率，我们发现MeCP2对转录伸长没有可测量的作用，而是抑制了Pol II启动高度甲基化的长基因转录的速率。
更新日期：2019-11-27
中文翻译：
MeCP2抑制高度甲基化的长基因的转录起始速率。
甲基-DNA结合阻遏蛋白MeCP2中的突变导致毁灭性神经发育障碍Rett综合征。理解MeCP2如何调节转录是一项挑战，因为MeCP2在整个基因组中广泛结合，并且MeCP2突变与神经元基因表达中普遍存在的小幅度变化有关。我们在这里证明MeCP2通过与NCoR协同阻遏物复合物的相互作用抑制大脑中高度甲基化的长基因的新生RNA转录。通过直接在大脑中测量转录起始和伸长的速率，我们发现MeCP2对转录伸长没有可测量的作用，而是抑制了Pol II启动高度甲基化的长基因转录的速率。
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