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HSF1 在耐旱性转录调控中的全基因组作用:以休眠细胞系 Pv11 为例。

Genome-Wide Role of HSF1 in Transcriptional Regulation of Desiccation Tolerance in the Anhydrobiotic Cell Line, Pv11.

机构信息

Department of Integrated Biosciences, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa 277-8562, Japan.

Division of Biotechnology, Institute of Agrobiological Sciences, National Agriculture and Food Research Organization (NARO), Tsukuba 305-0851, Japan.

出版信息

Int J Mol Sci. 2021 May 28;22(11):5798. doi: 10.3390/ijms22115798.

Abstract

The Pv11, an insect cell line established from the midge , is capable of extreme hypometabolic desiccation tolerance, so-called anhydrobiosis. We previously discovered that heat shock factor 1 (HSF1) contributes to the acquisition of desiccation tolerance by Pv11 cells, but the mechanistic details have yet to be elucidated. Here, by analyzing the gene expression profiles of newly established HSF1-knockout and -rescue cell lines, we show that HSF1 has a genome-wide effect on gene regulation in Pv11. The HSF1-knockout cells exhibit a reduced desiccation survival rate, but this is completely restored in HSF1-rescue cells. By comparing mRNA profiles of the two cell lines, we reveal that HSF1 induces anhydrobiosis-related genes, especially genes encoding late embryogenesis abundant proteins and thioredoxins, but represses a group of genes involved in basal cellular processes, thus promoting an extreme hypometabolism state in the cell. In addition, HSF1 binding motifs are enriched in the promoters of anhydrobiosis-related genes and we demonstrate binding of HSF1 to these promoters by ChIP-qPCR. Thus, HSF1 directly regulates the transcription of anhydrobiosis-related genes and consequently plays a pivotal role in the induction of anhydrobiotic ability in Pv11 cells.

摘要

从摇蚊中建立的昆虫细胞系 Pv11 能够实现极端的低代谢干燥耐受性,即所谓的脱水休眠。我们之前发现热休克因子 1(HSF1)有助于 Pv11 细胞获得干燥耐受性,但具体的机制细节尚未阐明。在这里,通过分析新建立的 HSF1 敲除和挽救细胞系的基因表达谱,我们表明 HSF1 对 Pv11 中的基因调控具有全基因组的影响。HSF1 敲除细胞表现出降低的干燥存活率,但在 HSF1 挽救细胞中完全恢复。通过比较这两种细胞系的 mRNA 谱,我们揭示了 HSF1 诱导了与脱水休眠相关的基因,特别是编码晚期胚胎丰富蛋白和硫氧还蛋白的基因,但抑制了一组涉及基础细胞过程的基因,从而促进了细胞的极度低代谢状态。此外,HSF1 结合基序在与脱水休眠相关的基因启动子中富集,我们通过 ChIP-qPCR 证明了 HSF1 与这些启动子的结合。因此,HSF1 直接调节与脱水休眠相关基因的转录,从而在 Pv11 细胞中诱导脱水休眠能力中发挥关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b7bf/8197945/46d56e02ad33/ijms-22-05798-g001.jpg

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