Thomas F Nguyen, James Z J Kwan, Jennifer E Mitchell, Jieying H Cui, Sheila S Teves
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引用次数: 0
摘要
细胞通过在转录和翻译水平上改变基因表达模式来应对许多不同类型的应激。在热胁迫下,全局转录和翻译受到抑制,而伴侣蛋白的表达受到优先支持。作为mRNA转录和蛋白翻译之间的直接联系,tRNA的表达在应激反应中受到复杂的调控。尽管对热休克反应(HSR)进行了广泛的研究,但在哺乳动物细胞中,RNA聚合酶III (Pol III)转录对tRNA表达的调控尚未完全阐明。在这里,我们研究了小鼠胚胎干细胞(mESCs)热休克应激不同阶段Pol III转录的调控。我们观察到,Pol III转录在热休克30分钟后下调,随后在热休克60分钟后转录整体增加。这种效应在trna中更为明显,尽管其他Pol III基因靶点也受到类似影响。值得注意的是,我们发现热休克30分钟时的下调与HSR的主转录因子HSF1无关,但随后在60分钟时表达的增加需要HSF1。综上所述,这些结果证明了RNA Pol III对热应激的适应性反应,以及典型HSR和tRNA表达之间的复杂关系。
Dynamic regulation of murine RNA polymerase III transcription during heat shock stress.
Cells respond to many different types of stresses by overhauling gene expression patterns, both at the transcriptional and translational levels. Under heat stress, global transcription and translation are inhibited, while the expression of chaperone proteins is preferentially favored. As the direct link between mRNA transcription and protein translation, transfer RNA (tRNA) expression is intricately regulated during the stress response. Despite extensive research into the heat shock response (HSR), the regulation of tRNA expression by RNA polymerase III (Pol III) transcription has yet to be fully elucidated in mammalian cells. Here, we examine the regulation of Pol III transcription during different stages of heat shock stress in mouse embryonic stem cells. We observe that Pol III transcription is downregulated after 30 min of heat shock, followed by an overall increase in transcription after 60 min of heat shock. This effect is more evident in tRNAs, although other Pol III gene targets are also similarly affected. Notably, we show that the downregulation at 30 min of heat shock is independent of HSF1, the master transcription factor of the HSR, but that the subsequent increase in expression at 60 min requires HSF1. Taken together, these results demonstrate an adaptive RNA Pol III response to heat stress and an intricate relationship between the canonical HSR and tRNA expression.
期刊介绍:
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