Identification of novel heat shock-induced long non-coding RNA in human cells

Identification of novel heat shock-induced long non-coding RNA in human cells
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人类细胞中新型热休克诱导的长非编码 RNA 的鉴定

DOI:
10.1093/jb/mvaa126
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发表时间:
2020
期刊:
The Journal of Biochemistry
影响因子:
--
通讯作者:
Akimitsu Nobuyoshi
Akimitsu Nobuyoshi
中科院分区:
--
文献类型:
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作者:
Onoguchi-Mizutani Rena;Kishi Yoshihiro;Ogura Yoko;Nishimura Yuuki;Imamachi Naoto;Suzuki Yutaka;Miyazaki Satoru;Akimitsu Nobuyoshi

文献摘要

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热休克反应是生物体在热应激条件下生存的重要系统。在热休克应激过程中,基因表达受到整体抑制,但某些基因的表达受到选择性的促进,如伴侣基因。这些选择性激活的基因在热激反应中起着关键作用,因此有必要发现热诱导基因来揭示整体的热激反应图景。热诱导蛋白编码基因的表达谱已经得到了很好的研究,但非编码基因在哺乳动物系统中的表达谱仍不清楚。在这里,我们使用对热休克处理的A549细胞的RNA-SEQ分析来识别七个对热休克有反应的新的长非编码RNA。我们对热休克诱导最显著的CTD-2377D24.6 RNA进行了研究,发现CTD-2377D24.6的启动子区域含有转录因子HSF1(热休克因子1)的结合位点,HSF1在热休克反应中起核心作用。我们证实,HSF1基因敲除取消了热休克时CTD-2377D24.6RNA的诱导。这些结果表明,CTD-2377D24.6RNA是一种新的热休克诱导的转录本,由HSF1转录。
The heat-shock response is a crucial system for survival of organisms under heat stress. During heat-shock stress, gene expression is globally suppressed, but expression of some genes, such as chaperone genes, is selectively promoted. These selectively activated genes have critical roles in the heat-shock response, so it is necessary to discover heat-inducible genes to reveal the overall heat-shock response picture. The expression profiling of heat-inducible protein-coding genes has been well-studied, but that of non-coding genes remains unclear in mammalian systems. Here, we used RNA-seq analysis of heat shock-treated A549 cells to identify seven novel long non-coding RNAs that responded to heat shock. We focussed on CTD-2377D24.6 RNA, which is most significantly induced by heat shock, and found that the promoter region of CTD-2377D24.6 contains the binding site for transcription factor HSF1 (heat shock factor 1), which plays a central role in the heat-shock response. We confirmed that HSF1 knockdown cancelled the induction of CTD-2377D24.6 RNA upon heat shock. These results suggest that CTD-2377D24.6 RNA is a novel heat shock-inducible transcript that is transcribed by HSF1.