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小分子热休克蛋白 Hsp67Bc 在冷应激耐受中发挥重要作用。

Small heat shock protein Hsp67Bc plays a significant role in cold stress tolerance.

机构信息

Cell Biology Department, Institute of Cytology and Genetics SB RAS, Novosibirsk 630090, Russia

Cell Biology Department, Institute of Cytology and Genetics SB RAS, Novosibirsk 630090, Russia.

出版信息

J Exp Biol. 2020 Nov 2;223(Pt 21):jeb219592. doi: 10.1242/jeb.219592.

Abstract

Hsp67Bc in is a member of the small heat shock protein family, the main function of which is to prevent the aggregation of misfolded or damaged proteins. Hsp67Bc interacts with Starvin and Hsp23, which are known to be a part of the cold stress response in the fly during the recovery phase. In this study, we investigated the role of the gene in the cold stress response. We showed that in adult , expression increases after cold stress and decreases after 1.5 h of recovery, indicating the involvement of Hsp67Bc in short-term stress recovery. We also implemented a deletion in the gene using imprecise excision of a -element, and analysed the cold tolerance of null mutants at different developmental stages. We found that null homozygous flies are viable and fertile but display varying cold stress tolerance throughout the stages of ontogenesis: the survival after cold stress is slightly impaired in late third instar larvae, unaffected in pupae, and notably affected in adult females. Moreover, the recovery from chill coma is delayed in null adults of both sexes. In addition, the deletion in the gene caused more prominent up-regulation of following cold stress, suggesting the involvement of in compensation of the lack of the Hsp67Bc protein. Taken together, our results suggest that Hsp67Bc is involved in the recovery of flies from a comatose state and contributes to the protection of the fruit fly from cold stress.

摘要

在果蝇中,Hsp67Bc 是小热休克蛋白家族的成员,其主要功能是防止错误折叠或受损蛋白质的聚集。Hsp67Bc 与 Starvin 和 Hsp23 相互作用,已知这两种蛋白在果蝇的恢复期参与冷应激反应。在这项研究中,我们研究了 基因在冷应激反应中的作用。我们发现,在成年果蝇中,冷应激后 Hsp67Bc 的表达增加,恢复 1.5 小时后表达减少,表明 Hsp67Bc 参与了短期应激恢复。我们还使用转座子的不精确切除在 基因中进行了缺失,并分析了不同发育阶段缺失突变体对冷胁迫的耐受性。我们发现,纯合缺失突变体果蝇是存活且可育的,但在整个个体发生过程中对冷胁迫的耐受性不同:晚期三龄幼虫的冷胁迫后存活率略有降低,蛹期不受影响,而成年雌性的存活率明显降低。此外,雌雄两性的 null 成虫从冷昏迷中恢复的时间都延迟了。此外,缺失 基因后,冷应激后 基因的上调更为显著,这表明 基因可能参与了 Hsp67Bc 蛋白缺失的补偿。总之,我们的研究结果表明,Hsp67Bc 参与了果蝇从昏迷状态中恢复,有助于保护果蝇免受冷应激的伤害。

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