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在Caenorhabditis elegans中,OSM-11调节了盐度压力耐受性

Pengchi Zhang^1,2,3,4,5, Beining Xue^1,2,3,4, Yusu Xie^1,2,3

¹CAS and Shandong Province Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao, 266071, China.

bioRxiv : the preprint server for biology

|December 3, 2025

概括

osm-11基因的突变通过改变脂肪酸代谢和信号来增强C. elegans的盐度应激抵抗力. 这项研究揭示了在高盐度条件下参与动物生存的关键分子通路.

科学领域:

分子生物学分子生物学
遗传学遗传学是一个
环境科学环境科学

背景情况:

与海洋物种相比,陆地动物一般具有有限的盐分耐受性.
编码Notch协同连接体的osm-11基因与C. elegans的超盐耐受性有关,但根本机制尚未完全理解.

研究的目的:

阐明OSM-11突变赋予C. elegans增强的盐度应激抵抗力的分子机制.
为了确定由osm-11调节的特定代谢和信号通路,以应对盐度压力.

主要方法:

用RNA测序分析了对OSM-11突变的基因表达变化的反应.
使用CRISPR/Cas-9基因组编辑来创建和研究特定的基因淘汰.
进行了形态分析,观察细胞的变化,特别是线粒体结构和脂质滴.

主要成果:

Osm-11突变调高脂肪酸代谢 (例如,acdh-12,acs-17) 和细胞染色体P450通路 (例如,ugt-15),同时抑制信号传递.
在acdh-12中发生的突变通过激活ferroptosis和mitophagy,降低氧化酸化的调节,并提高自的调节,损害了盐分耐受性.
线粒体碎片化有助于高盐度下野生类型的死亡率,脂质滴滴积累与降低β-氧化基因表达相关.

结论:

Osm-11调节复杂的途径网络,包括脂肪酸代谢,信号传递和细胞应激反应,以调节盐分耐受性.
了解这些机制为制定保护动物免受环境度压力因素的策略提供了洞察力.

关键词:

在ACDH-12中使用.脂肪酸的代谢脂肪酸的代谢铁性化 (ferroptosis) 是一种线粒细胞衰变 (mitophagy) 是一种神经衰变的过程.在OSM-11中使用.盐度-压力耐受性耐受性

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