在"冬眠"中重新编程基因表达C. elegans涉及到 IRE-1/XBP-1 路径
Melanie Lianne Engelfriet1, Yanwu Guo1, Andreas Arnold2,3
1Section for Biochemistry and Molecular Biology, Department of Biosciences, University of Oslo, Oslo, Norway.
eLife
|May 6, 2025
概括
细胞通过调节转录水平的基因表达而不是蛋白质合成来生存. 展开的蛋白质反应 (UPR) 途径有助于寒冷适应和生存.
科学领域:
- 分子生物学分子生物学
- 细胞应激反应的细胞应激反应
- 低温生物学 低温生物学
背景情况:
- 动物冬眠和临床低温被用于医疗治疗,但细胞寒冷生存机制仍然不清楚.
- 全球蛋白质合成下调是一种已知的寒冷适应策略,但其作用仍在争论中.
- 了解寒冷适应对于从进化生物学到急诊医学等领域至关重要.
研究的目的:
- 为了研究细胞寒冷生存的分子机制.
- 为了确定冷暴露期间蛋白质合成和基因表达是如何调节的.
- 确定参与寒冷适应的关键信号通路.
主要方法:
- 研究了线虫 *Caenorhabditis elegans* 的寒冷适应性.
- 在低温度下分析信使RNA (mRNA) 翻译速率.
- 研究了基因表达模式和未折叠蛋白质反应 (UPR) 的作用.
- 检查了 IRE-1/XBP-1 信号通路在冷诱导基因表达中的参与.
主要成果:
- 在C. elegans中,大多数mRNA在寒冷中继续翻译,尽管速度较低.
- 感冒特异性基因表达主要在转录水平上受到调节.
- 通过IRE-1/XBP-1通路,展开的蛋白质反应 (UPR) 被冷气激活.
- 这种UPR通路的激活与寒冷诱导的内质网膜应激有关.
- 通过IRE-1/XBP-1信号的UPR激活增强了感冒生存.
结论:
- *C. elegans*的寒冷适应依赖于转录调节,而不是全球翻译关闭.
- 展开的蛋白质反应 (UPR) 作为一个关键的寒冷生存机制.
- 感冒引起的ER压力触发了IRE-1/XBP-1通路,促进了细胞的弹性.
- 这项研究揭示了UPR在寒冷适应和生存中的新角色.
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