Department of Microbiology, Oslo University Hospital, NO-0027 Oslo, Norway.
Department of Molecular Cell Biology, Institute for Cancer Research, the Norwegian Radium Hospital, Montebello, N-0379 Oslo, Norway; Section for Biochemistry and Molecular Biology, Faculty of Mathematics and Natural Sciences, University of Oslo, 0371, Norway.
Biochim Biophys Acta Gene Regul Mech. 2018 Apr;1861(4):310-319. doi: 10.1016/j.bbagrm.2017.11.001. Epub 2017 Nov 7.
RNA polymerase III (RNAPIII) transcribes tRNA genes, 5S RNA as well as a number of other non-coding RNAs. Because transcription by RNAPIII is an energy-demanding process, its activity is tightly linked to the stress levels and nutrient status of the cell. Multiple signaling pathways control RNAPIII activity in response to environmental cues, but exactly how these pathways regulate RNAPIII is still poorly understood. One major target of these pathways is the transcriptional repressor Maf1, which inhibits RNAPIII activity under conditions that are detrimental to cell growth. However, recent studies have found that the cell can also directly regulate the RNAPIII machinery through phosphorylation and sumoylation of RNAPIII subunits. In this review we summarize post-translational modifications of RNAPIII subunits that mainly have been identified in large-scale proteomics studies, and we highlight several examples to discuss their relevance for regulation of RNAPIII.
RNA 聚合酶 III(RNAPIII)转录 tRNA 基因、5S RNA 以及许多其他非编码 RNA。由于 RNAPIII 的转录是一个耗能过程,其活性与细胞的应激水平和营养状态紧密相关。多种信号通路控制 RNAPIII 的活性以响应环境线索,但这些通路如何调节 RNAPIII 的机制仍知之甚少。这些通路的一个主要靶标是转录抑制剂 Maf1,它在不利于细胞生长的条件下抑制 RNAPIII 的活性。然而,最近的研究发现,细胞还可以通过 RNAPIII 亚基的磷酸化和 sumoylation 直接调节 RNAPIII 机制。在这篇综述中,我们总结了主要在大规模蛋白质组学研究中鉴定出的 RNAPIII 亚基的翻译后修饰,并强调了几个例子来讨论它们对 RNAPIII 调节的相关性。