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首页> 外文期刊>Molecular and Cellular Biology >Transcription-Coupled Methylation of Histone H3 at Lysine 36 Regulates Dosage Compensation by Enhancing Recruitment of the MSL Complex in Drosophila melanogaster
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Transcription-Coupled Methylation of Histone H3 at Lysine 36 Regulates Dosage Compensation by Enhancing Recruitment of the MSL Complex in Drosophila melanogaster

机译：赖氨酸36的组蛋白H3的转录偶联甲基化通过增强果蝇MSL复合物的募集来调节剂量补偿。

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In Drosophila melanogaster, dosage compensation relies on the targeting of the male-specific lethal (MSL) complex to hundreds of sites along the male X chromosome. Transcription-coupled methylation of histone H3 lysine 36 is enriched toward the 3′ end of active genes, similar to the MSL proteins. Here, we have studied the link between histone H3 methylation and MSL complex targeting using RNA interference and chromatin immunoprecipitation. We show that trimethylation of histone H3 at lysine 36 (H3K36me3) relies on the histone methyltransferase Hypb and is localized promoter distal at dosage-compensated genes, similar to active genes on autosomes. However, H3K36me3 has an X-specific function, as reduction specifically decreases acetylation of histone H4 lysine 16 on the male X chromosome. This hypoacetylation is caused by compromised MSL binding and results in a failure to increase expression twofold. Thus, H3K36me3 marks the body of all active genes yet is utilized in a chromosome-specific manner to enhance histone acetylation at sites of dosage compensation.
机译：在果蝇（Drosophila melanogaster）中，剂量补偿依赖于雄性特异性致死（MSL）复合物靶向雄性X染色体上数百个位点。与MSL蛋白相似，组蛋白H3赖氨酸36的转录偶联甲基化在活性基因的3'端富集。在这里，我们研究了使用RNA干扰和染色质免疫沉淀的组蛋白H3甲基化与MSL复合物靶向之间的联系。我们显示，赖氨酸36（H3K36me3）上的组蛋白H3的三甲基化依赖于组蛋白甲基转移酶Hypb，并且位于剂量补偿基因远端的启动子，类似于常染色体上的活性基因。但是，H3K36me3具有X特异功能，因为还原特异性降低了男性X染色体上组蛋白H4赖氨酸16的乙酰化。这种低乙酰化是由受损的MSL结合引起的，导致无法将表达增加两倍。因此，H3K36me3标记了所有活性基因的主体，但仍以染色体特异性方式用于增强剂量补偿位点处的组蛋白乙酰化。

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