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热休克在模式共生刺胞动物艾氏海葵中诱导宿主蛋白质稳态破坏和内质网应激。

Thermal Shock Induces Host Proteostasis Disruption and Endoplasmic Reticulum Stress in the Model Symbiotic Cnidarian Aiptasia.

作者信息

Oakley Clinton A, Durand Elysanne, Wilkinson Shaun P, Peng Lifeng, Weis Virginia M, Grossman Arthur R, Davy Simon K

机构信息

School of Biological Sciences, Victoria University of Wellington , Wellington 6012, New Zealand.

Department of Ecology and Environmental Sciences, Université Pierre et Marie Curie , Paris 75005, France.

出版信息

J Proteome Res. 2017 Jun 2;16(6):2121-2134. doi: 10.1021/acs.jproteome.6b00797. Epub 2017 May 11.

Abstract

Coral bleaching has devastating effects on coral survival and reef ecosystem function, but many of the fundamental cellular effects of thermal stress on cnidarian physiology are unclear. We used label-free liquid chromatography-tandem mass spectrometry to compare the effects of rapidly (33.5 °C, 24 h) and gradually (30 and 33.5 °C, 12 days) elevated temperatures on the proteome of the model symbiotic anemone Aiptasia. We identified 2133 proteins in Aiptasia, 136 of which were differentially abundant between treatments. Thermal shock, but not acclimation, resulted in significant abundance changes in 104 proteins, including those involved in protein folding and synthesis, redox homeostasis, and central metabolism. Nineteen abundant structural proteins showed particularly reduced abundance, demonstrating proteostasis disruption and potential protein synthesis inhibition. Heat shock induced antioxidant mechanisms and proteins involved in stabilizing nascent proteins, preventing protein aggregation and degrading damaged proteins, which is indicative of endoplasmic reticulum stress. Host proteostasis disruption occurred before either bleaching or symbiont photoinhibition was detected, suggesting host-derived reactive oxygen species production as the proximate cause of thermal damage. The pronounced abundance changes in endoplasmic reticulum proteins associated with proteostasis and protein turnover indicate that these processes are essential in the cellular response of symbiotic cnidarians to severe thermal stress.

摘要

珊瑚白化对珊瑚生存和珊瑚礁生态系统功能具有毁灭性影响,但热应激对刺胞动物生理学的许多基本细胞效应尚不清楚。我们使用无标记液相色谱 - 串联质谱法比较了快速(33.5°C,24小时)和逐渐(30和33.5°C,12天)升温对模式共生海葵艾氏海葵蛋白质组的影响。我们在艾氏海葵中鉴定出2133种蛋白质,其中136种在不同处理之间丰度存在差异。热休克而非驯化导致104种蛋白质的丰度发生显著变化,包括参与蛋白质折叠与合成、氧化还原稳态和中心代谢的蛋白质。19种丰富的结构蛋白丰度尤其降低,表明蛋白质稳态破坏和潜在的蛋白质合成抑制。热休克诱导了抗氧化机制以及参与稳定新生蛋白质、防止蛋白质聚集和降解受损蛋白质的蛋白质,这表明存在内质网应激。在检测到白化或共生体光抑制之前就发生了宿主蛋白质稳态破坏,这表明宿主产生的活性氧是热损伤的直接原因。与蛋白质稳态和蛋白质周转相关的内质网蛋白质丰度的显著变化表明,这些过程在共生刺胞动物对严重热应激的细胞反应中至关重要。

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