Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada.
Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Curr Genet. 2021 Oct;67(5):695-705. doi: 10.1007/s00294-021-01196-x. Epub 2021 Jun 5.
Co-transcriptional histone modifications are a ubiquitous feature of RNA polymerase II (RNAPII) transcription, with profound but incompletely understood effects on gene expression. Unlike the covalent marks found at promoters, which are thought to be instructive for transcriptional activation, these modifications occur in gene bodies as a result of transcription, which has made elucidation of their functions challenging. Here we review recent insights into the regulation and roles of two such modifications: monoubiquitylation of histone H2B at lysine 120 (H2Bub1) and methylation of histone H3 at lysine 36 (H3K36me). Both H2Bub1 and H3K36me are enriched in the coding regions of transcribed genes, with highly overlapping distributions, but they were thought to work largely independently. We highlight our recent demonstration that, as was previously shown for H3K36me, H2Bub1 signals to the histone deacetylase (HDAC) complex Rpd3S/Clr6-CII, and that Rpd3S/Clr6-CII and H2Bub1 function in the same pathway to repress aberrant antisense transcription initiating within gene coding regions. Moreover, both of these histone modification pathways are influenced by protein phosphorylation catalyzed by the cyclin-dependent kinases (CDKs) that regulate RNAPII elongation, chiefly Cdk9. Therefore, H2Bub1 and H3K36me are more tightly linked than previously thought, sharing both upstream regulatory inputs and downstream effectors. Moreover, these newfound connections suggest extensive, bidirectional signaling between RNAPII elongation complexes and chromatin-modifying enzymes, which helps to determine transcriptional outputs and should be a focus for future investigation.
共转录组蛋白修饰是 RNA 聚合酶 II(RNAPII)转录的普遍特征,对基因表达具有深远但不完全理解的影响。与启动子处发现的作为转录激活指导的共价标记不同,这些修饰发生在基因体中,这使得它们的功能阐明具有挑战性。在这里,我们回顾了最近关于两种修饰的调节和作用的见解:组蛋白 H2B 赖氨酸 120 单泛素化(H2Bub1)和组蛋白 H3 赖氨酸 36 甲基化(H3K36me)。H2Bub1 和 H3K36me 在转录基因的编码区中丰富,具有高度重叠的分布,但它们被认为主要独立工作。我们强调了我们最近的证明,即正如之前对 H3K36me 所示,H2Bub1 向组蛋白去乙酰化酶(HDAC)复合物 Rpd3S/Clr6-CII 发出信号,并且 Rpd3S/Clr6-CII 和 H2Bub1 在相同的途径中发挥作用,以抑制起始于基因编码区的异常反义转录。此外,这两种组蛋白修饰途径都受到细胞周期蛋白依赖性激酶(CDKs)催化的蛋白质磷酸化的影响,CDKs 调节 RNAPII 延伸,主要是 Cdk9。因此,H2Bub1 和 H3K36me 比以前认为的更紧密地联系在一起,它们共享上游调节输入和下游效应器。此外,这些新发现的联系表明,RNAPII 延伸复合物和染色质修饰酶之间存在广泛的双向信号传递,这有助于确定转录输出,应该成为未来研究的重点。