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Oxidative stress is an essential factor for the induction of anhydrobiosis in the desiccation-tolerant midge, Polypedilum vanderplanki (Diptera, Chironomidae)
Mitochondrion ( IF 4.4 ) Pub Date : 2023-11-11 , DOI: 10.1016/j.mito.2023.11.002
Richard Cornette 1 , Hiroko P Indo 2 , Ken-Ichi Iwata 1 , Yuka Hagiwara-Komoda 3 , Yuichi Nakahara 4 , Oleg Gusev 5 , Takahiro Kikawada 1 , Takashi Okuda 6 , Hideyuki J Majima 7
Affiliation  

The sleeping chironomid (Polypedilum vanderplanki) is the only insect capable of surviving complete desiccation in an ametabolic state called anhydrobiosis. Here, we focused on the role of oxidative stress and we observed the production of reactive oxygen species (ROS) in desiccating larvae and in those exposed to salinity stress. Oxidative stress occurs to some extent in desiccating larvae, inducing carbonylation of proteins. Oxidative stress overcomes the antioxidant defenses of the larvae during the first hour following rehydration of anhydrobiotic larvae. It facilitates the oxidation of DNA and cell membrane lipids; however, these damages are quickly repaired after a few hours. In addition to its deleterious effects, we demonstrated that artificial exposure to oxidative stress could induce a response similar to desiccation stress, at the transcriptome and protein levels. Furthermore, the response of anhydrobiosis-related genes to desiccation and salinity stress was inhibited by antioxidant treatment. Thus, we conclude that oxidative stress is an essential trigger for inducing the expression of protective genes during the onset of anhydrobiosis in desiccating of P. vanderplanki larvae.



中文翻译:

氧化应激是耐干燥蠓(Polypedilum vanderplanki)(双翅目、摇蚊科)诱导脱水的重要因素

睡眠中的摇蚊(Polypedilum vanderplanki)是唯一能够在称为“脱水生物”的代谢状态下完全干燥后存活的昆虫。在这里,我们重点关注氧化应激的作用,并观察了干燥幼虫和暴露于盐度应激的幼虫中活性氧(ROS)的产生。氧化应激在一定程度上发生在幼虫干燥过程中,诱导蛋白质的羰基化。在脱水幼虫补水后的第一个小时内,氧化应激克服了幼虫的抗氧化防御。促进DNA和细胞膜脂质的氧化;然而,这些损坏会在几个小时后迅速修复。除了其有害影响之外,我们还证明,人工暴露于氧化应激可能会在转录组和蛋白质水平上引起类似于干燥应激的反应。此外,抗氧化处理抑制了脱水相关基因对干燥和盐度胁迫的反应。因此,我们得出结论,氧化应激是范德普兰基幼虫脱水过程中诱导保护基因表达的重要触发因素。

更新日期:2023-11-11
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