从核糖体基因解释非编码rna的起源和功能

IF 4 2区 生物学 Q2 CELL BIOLOGY
Tom Moss, Dany S. Sibai, Frédéric Lessard
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引用次数: 0

摘要

哺乳动物的核糖体DNA (rDNA)被组织成大的串联重复序列簇,每个重复序列编码18S、5.8S和28S核糖体rna (rrna)的单个47S前体,rrna在上游和下游两侧由一个基因间间隔(IGS),最初被称为非转录间隔(NTS)。然而,在某些细胞和某些环境条件下,IGS被发现低水平转录以产生一系列“非编码”rna (ncRNAs)。这些ncrna参与了rRNA合成、rDNA沉默和蛋白质隔离的调控,以响应环境和致癌应激以及肿瘤抑制。在这里,我们回顾了这些ncrna的产生、调控和潜在功能的数据。我们认为,大多数ncrna起源于Reb1和myb相关转录“路障”因子TTF1的RNA聚合酶I转录终止失败,并将其表达与肿瘤抑制联系起来。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Interpreting the Origins and Functions of Noncoding RNAs From the Ribosomal Genes

Interpreting the Origins and Functions of Noncoding RNAs From the Ribosomal Genes

The Ribosomal DNA (rDNA) in mammals is organised into large clusters of tandem repeats each of which encodes a single 47S precursor for the 18S, 5.8S, and 28S ribosomal RNAs (rRNAs) that is flanked upstream and downstream by an Intergenic Spacer (IGS) originally referred to as the Non-Transcribed Spacer (NTS). However, in certain cells and under certain environmental conditions the IGS has been found to be transcribed at low level to generate a range of “Noncoding” RNAs (ncRNAs). These ncRNAs have been implicated in the regulation of rRNA synthesis, rDNA silencing and protein sequestration in response to environmental and oncogenic stresses and tumour suppression. Here we review data on the generation, regulation and potential functions of these ncRNAs. We suggest that the majority of the ncRNAs originate from a failure of RNA polymerase I transcription termination by the Reb1- and Myb-related transcriptional “road-block” factor TTF1 and link their expression with tumour suppression.

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来源期刊
CiteScore
14.70
自引率
0.00%
发文量
256
审稿时长
1 months
期刊介绍: The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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