Mitochondrial ROS signalling requires uninterrupted electron flow and is lost during ageing in flies.

Mitochondrial ROS signalling requires uninterrupted electron flow and is lost during ageing in flies.
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DOI:
10.1007/s11357-022-00555-x
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发表时间:
2022-08
期刊:
影响因子:
5.6
通讯作者:
Sanz, Alberto
Sanz, Alberto
中科院分区:
医学1区
文献类型:
--
作者:
Graham, Charlotte;Stefanatos, Rhoda;Yek, Angeline E. H.;Spriggs, Ruth, V;Loh, Samantha H. Y.;Uribe, Alejandro Huerta;Zhang, Tong;Martins, L. Miguel;Maddocks, Oliver D. K.;Scialo, Filippo;Sanz, Alberto

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线粒体活性氧(mitochondrialreactiveoxygenspecies,mtROS)是维持细胞内环境稳定的重要信使。响应于应激,通过呼吸复合物I的反向电子传递(RET)产生高水平的mtROS。通过RET(ROS-RET)抑制ROS产生降低了应激下的存活率,而ROS-RET的激活延长了基础条件下的寿命。在这里,我们证明了ROS-RET信号需要增加电子进入和不间断的电子流通过电子传递链(ETC)。我们发现,在老年果蝇中,当电子通量减少时,ROS-RET被废除,并且它们的线粒体持续产生高水平的mtROS。最后,我们证明,在年轻的苍蝇,限制电子出口,但不进入,从ETC phenocopies mtROS一代观察到在老年人。我们的研究结果阐明了ROS信号在衰老过程中丢失的机制。在线版本包含补充材料,可通过10.1007/s11357-022-00555-x获得。
Mitochondrial reactive oxygen species (mtROS) are cellular messengers essential for cellular homeostasis. In response to stress, reverse electron transport (RET) through respiratory complex I generates high levels of mtROS. Suppression of ROS production via RET (ROS-RET) reduces survival under stress, while activation of ROS-RET extends lifespan in basal conditions. Here, we demonstrate that ROS-RET signalling requires increased electron entry and uninterrupted electron flow through the electron transport chain (ETC). We find that in old fruit flies, ROS-RET is abolished when electron flux is decreased and that their mitochondria produce consistently high levels of mtROS. Finally, we demonstrate that in young flies, limiting electron exit, but not entry, from the ETC phenocopies mtROS generation observed in old individuals. Our results elucidate the mechanism by which ROS signalling is lost during ageing. The online version contains supplementary material available at 10.1007/s11357-022-00555-x.
TORC2通过促进应激颗粒的形成来介导果蝇中的热应力反应。
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