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快速的体重恢复、代谢率调整和基因表达调控定义了冷应激蜜蜂幼虫的反应。

Fast weight recovery, metabolic rate adjustment and gene-expression regulation define responses of cold-stressed honey bee brood.

机构信息

Laboratorio de Fisiología Molecular e Integrativa, Instituto de Investigaciones Biológicas (IIB), Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET) - Universidad Nacional de Mar del Plata (UNMdP), CC1245, 7600 Mar del Plata, Argentina.

Laboratorio de Ecología Fisiológica y del Comportamiento, Instituto de Investigaciones Marinas y Costeras (IIMyC), CONICET - UNMdP, 7600 Mar del Plata, Argentina.

出版信息

J Insect Physiol. 2021 Jan;128:104178. doi: 10.1016/j.jinsphys.2020.104178. Epub 2020 Dec 5.

Abstract

In temperate climates, low ambient temperatures in late winter and in spring can result in cold stress conditions in brood areas of weakened honey bee colonies, leading to increased levels of developmental interruptions and death of the brood. Very little is known about the physiological and molecular mechanisms that regulate honey bee brood responses to acute cold-stress. Here, we hypothesized that central regulatory pathways mediated by insulin/insulin-like peptide signalling (IIS) and adipokinetic hormone (AKH) are linked to metabolic changes in cold-stressed honey bee brood. A. mellifera brood reared at suboptimal temperatures showed diminished growth rate and arrested development progress. Notably, cold-stressed brood rapidly recovers the growth in the first 24 h after returning at control rearing temperature, sustained by the induction of compensatory mechanisms. We determined fast changes in the expression of components of IIS and AKH pathways in cold-stressed brood supporting their participation in metabolic events, growth and stress responses. We also showed that metabolic rate keeps high in brood exposed to stress suggesting a role in energy supply for growth and cell repair. Additionally, transcript levels of the uncoupling protein MUP2 were elevated in cold-stressed brood, which could indicate that this protein acts in the heat generation through mitochondrial decoupling mechanisms and/or in the ROS attenuation. Physiological, metabolic and molecular mechanisms that shape the responses to cold-stress in honey bee brood are addressed and discussed.

摘要

在温带气候中,冬季末和春季的环境温度较低,可能会导致弱势蜜蜂群体的育雏区出现冷应激条件,导致幼虫发育中断和死亡的水平增加。对于调节蜜蜂幼虫对急性冷应激的反应的生理和分子机制,我们知之甚少。在这里,我们假设由胰岛素/胰岛素样肽信号(IIS)和激动素(AKH)介导的中央调节途径与冷应激蜜蜂幼虫的代谢变化有关。在亚最佳温度下饲养的 A. mellifera 幼虫表现出生长速度减慢和发育进度停滞。值得注意的是,冷应激的幼虫在返回控制饲养温度后的头 24 小时内迅速恢复生长,这得益于补偿机制的诱导。我们确定了冷应激幼虫中 IIS 和 AKH 途径成分的快速表达变化,支持它们参与代谢事件、生长和应激反应。我们还表明,在应激下暴露的幼虫的代谢率保持较高,这表明其在生长和细胞修复的能量供应中发挥作用。此外,在冷应激的幼虫中,解偶联蛋白 MUP2 的转录水平升高,这可能表明该蛋白通过线粒体解偶联机制和/或在 ROS 衰减中发挥作用。本文探讨和讨论了塑造蜜蜂幼虫对冷应激反应的生理、代谢和分子机制。

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