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依赖于网红素的ER-phagy调解了C. elegans中对热应激的适应

Claudia Serot¹, Vincent Scarcelli², Alexandre Pouget³

¹Institute for Integrative Biology of the Cell (I2BC), CEA, CNRS, Univ. Paris-Sud Université Paris-Saclay, Gif-sur-Yvette cedex 91198, France; Department of R&I in Monogastric Animal Nutrition, European Laboratory of Innovation Science & Expertise (ELISE), Adisseo France S.A.S., Saint Fons 69190, France.

Current biology : CB

|May 6, 2025

概括

研究人员发现了一种新形式的ER-phagy,一种细胞清理过程,涉及RET-1d蛋白质. 这一过程有助于动物通过降解神经元和表皮中受损的内 плазма网膜 (ER) 来适应热应激.

科学领域:

细胞生物学细胞生物学
自学研究自学研究
应激反应机制应激反应机制

背景情况:

细胞内膜网膜 (ER) 稳态对于细胞功能至关重要.
自,一种细胞降解过程,通过ER-phagy在维持ER平衡中发挥作用.
不同类型的ER-phagy利用特定的自受体,这取决于ER压力因素.

研究的目的:

确定涉及ER-phagy的新机制和受体.
研究ER-phagy在适应急性热应激中的作用.
为了阐明在ER-phagy中网膜长异型 (RET-1d) 的功能.

主要方法:

在C. elegans中通过热应激诱导宏ER-phagy.
作为ER-phagy受体的RET-1d蛋白的识别和表征.
使用LC3相互作用区域 (LIR) 动机分析RET-1d与LGG-1/GABARAP的相互作用.
对RET-1d和LIR进行枯竭和突变研究,以评估ER-phagy功能.
评估动物适应热应激的能力.

主要成果:

在热应激期间由管状ER碎片化诱导的新型宏ER-phagy通路被确定.
连网素长异型 (RET-1d) 被确定为一个关键的ER-phagy受体,主要表达在神经系统和表皮.
RET-1d通过两个LIR基因与自蛋白LGG-1/GABARAP相互作用.
RET-1d的耗尽或其LIRs的突变损害了ER-phagy并减少了热应激适应.
揭示了神经元和表皮中的依赖RET-1d和LG-1的ER-phagy机制.

结论:

在热应激的反应中,RET-1d作为一个关键的受体,调解ER-phagy.
这种依赖RET-1d/LGG-1的ER-phagy通路对于在压力下神经元和表皮功能至关重要.
鉴定到的ER-phagy机制对C. elegans适应急性热应激有显著的贡献.

关键词:

压力ERER压力ERER压力在LGG-1/Gabarap中使用.一个LIR图案.在RET-1的异构形式中.自吸菌体自吸菌体自吸菌体自自是自的过程.发展发展发展发展发展.细胞内膜网膜的内oplasmic网膜.机车运动机车运动神经元神经元的神经元

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