胚胎细胞中的DNA损伤会诱导一种天生的免疫反应,从而触发系统性应激抵抗
Maria A Ermolaeva1, Alexandra Segref, Alexander Dakhovnik
1Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases, Institute for Genetics, University of Cologne, Zülpicher Strasse 47a, 50674 Cologne, Germany.
Nature
|August 27, 2013
概括
生殖细胞中的DNA损伤会在C. elegans体质组织中引发系统性应激抵抗. 这种由MPK-1和先天免疫调解的反应增强了蛋白质静止和生物体的耐力.
科学领域:
- 细胞和分子生物学 细胞和分子生物学
- 遗传学和基因组学 在
- 发育生物学 发展生物学
背景情况:
- 对于维持基因组稳定性而言,DNA损伤反应至关重要.
- 细胞自主检查点 (细胞循环停止,衰老,亡) 已得到充分研究.
- 对组织特异性基因组不稳定性的系统性反应尚不清楚,特别是在转基因后体质组织中.
研究的目的:
- 调查生殖细胞中的基因组不稳定性如何影响Caenorhabditis elegans体质组织.
- 阐明系统性抗压力的基础分子机制.
- 了解这种反应的适应意义.
主要方法:
- 在生殖细胞 (外源和内源) 中诱导DNA损伤.
- 评估体质组织对热和氧化应激的抵抗力.
- 分析ERK MAP激酶MPK-1和天生的免疫路径的作用.
- 在体组织中研究无素-蛋白酶体系统 (UPS) 激活.
主要成果:
- 胚胎细胞中的DNA损伤使体质组织中对热和氧化应激产生较高的抵抗力.
- 胚胎细胞中的ERK MAP激酶MPK-1介导这种体质应激抵抗.
- MPK-1信号传导诱导与先天免疫相关的假定分泌.
- 天生的免疫能激活体质组织中的全素-蛋白酶体系统 (UPS),增强蛋白质稳定性和系统性应激抵抗力.
结论:
- 生殖系基因组的不稳定性可以诱导体质组织中的全身应激反应.
- 这种反应涉及胚胎MPK-1信号传递,天生的免疫力和体质UPS激活.
- 拟议的适应性策略允许体质组织承受压力,在生殖细胞受到损害时延迟繁殖.
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