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细胞对线粒体的保护

摘要 : 美国哈佛医学院遗传系的研究人员研究细胞应激反应,揭示称为线粒体的细胞间如何使用周围的代谢物和微生物的信息,以保护自己免受伤害。相关文章发表于2014年4月9日的《Nature》杂志上。

线粒体(通过呼吸产生能量的细胞器)受损会触发各种保护性程序,但我们对监测线粒体功能和将其耦合到保护措施的信号作用通道却知之甚少。

通过对线虫进行全基因组RNA干涉筛选,Gary Ruvkun及同事识别出在线粒体受到由药物介导的基因破坏之后在上调保护性通道中所涉及的45个基因。

受这些基因影响、与监测相关的通道包括信号作用脂质“神经酰胺”的生物合成以及甲羟戊酸通道(该通道被能降低胆固醇的药物“斯达汀”抑制)。

原文摘要:

Caenorhabditis elegans pathways that surveil and defend mitochondria

Ying Liu, Buck S. Samuel, Peter C. Breen & Gary Ruvkun

Mitochondrial function is challenged by toxic by-products of me-tabolism as well as by pathogen attack. Caenorhabditis elegans normally responds to mitochondrial dysfunction with activation of mitochondrial-repair, drug-detoxification and pathogen-response pathways. Here, from a genome-wide RNA interference (RNAi) screen, we identified 45 C. elegans genes that are required to upregulate detoxification, pathogen-response and mitochondrial-repair pathways after inhibition of mitochondrial function by drug-induced or genetic disruption. Animals defective in ceramide biosynthesis are deficient in mitochondrial surveillance, and addition of particular ceramides can rescue the surveillance defects. Ceramide can also rescue the mitochondrial surveillance defects of other gene inactivations, mapping these gene activities upstream of ceramide. Inhibition of the meva1onate pathway, either by RNAi or statin drugs, also disrupts mitochondrial surveillance. Growth of C. elegans with a significant fraction of bacterial species from their natural habitat causes mitochondrial dysfunction. Other bacterial species inhibit C. elegansdefence responses to a mitochondrial toxin, revealing bacterial countermeasures to animal defence.

对应Nature杂志: 2014年4月17日Nature杂志精选

来源: Nature中文 浏览次数:187

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