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Insect mitochondria as targets of freezing-induced injury
Proceedings of the Royal Society B: Biological Sciences ( IF 4.7 ) Pub Date : 2020-07-22 , DOI: 10.1098/rspb.2020.1273 T Štětina 1, 2 , L E Des Marteaux 1 , V Koštál 1
Proceedings of the Royal Society B: Biological Sciences ( IF 4.7 ) Pub Date : 2020-07-22 , DOI: 10.1098/rspb.2020.1273 T Štětina 1, 2 , L E Des Marteaux 1 , V Koštál 1
Affiliation
Many insects survive internal freezing, but the great complexity of freezing stress hinders progress in understanding the ultimate nature of freezing-induced injury. Here, we use larvae of the drosophilid fly, Chymomyza costata to assess the role of mitochondrial responses to freezing stress. Respiration analysis revealed that fat body mitochondria of the freeze-sensitive (non-diapause) phenotype significantly decrease oxygen consumption upon lethal freezing stress, while mitochondria of the freeze-tolerant (diapausing, cold-acclimated) phenotype do not lose respiratory capacity upon the same stress. Using transmission electron microscopy, we show that fat body and hindgut mitochondria swell, and occasionally burst, upon exposure of the freeze-sensitive phenotype to lethal freezing stress. By contrast, mitochondrial swelling is not observed in the freeze-tolerant phenotype exposed to the same stress. We hypothesize that mitochondrial swelling results from permeability transition of the inner mitochondrial membrane and loss of its barrier function, which causes osmotic influx of cytosolic water into the matrix. We therefore suggest that the phenotypic transition to diapause and cold acclimation could be associated with adaptive changes that include the protection of the inner mitochondrial membrane against permeability transition and subsequent mitochondrial swelling. Accumulation of high concentrations of proline and other cryoprotective substances might be a part of such adaptive changes as we have shown that freezing-induced mitochondrial swelling was abolished by feeding the freeze-sensitive phenotype larvae on a proline-augmented diet.
中文翻译:
昆虫线粒体作为冷冻诱导损伤的靶点
许多昆虫在内部冷冻中存活下来,但冷冻应激的巨大复杂性阻碍了对冷冻诱导损伤的最终性质的理解。在这里,我们使用果蝇幼虫 Chymomyza costata 来评估线粒体对冷冻应激反应的作用。呼吸分析显示,冷冻敏感(非滞育)表型的脂肪体线粒体在致死性冷冻应激下显着降低耗氧量,而耐冻(滞育、冷驯化)表型的线粒体在相同情况下不会失去呼吸能力。压力。使用透射电子显微镜,我们显示脂肪体和后肠线粒体在冷冻敏感表型暴露于致命的冷冻应激时膨胀,偶尔会破裂。相比之下,在暴露于相同压力的耐冻表型中未观察到线粒体肿胀。我们假设线粒体肿胀是由线粒体内膜的通透性转变及其屏障功能丧失引起的,这导致细胞溶质水渗透流入基质。因此,我们认为向滞育和冷驯化的表型转变可能与适应性变化有关,包括保护线粒体内膜免受通透性转变和随后的线粒体肿胀。高浓度脯氨酸和其他冷冻保护物质的积累可能是这种适应性变化的一部分,因为我们已经表明,通过在脯氨酸增强饮食中喂养冷冻敏感表型幼虫,可以消除冷冻诱导的线粒体肿胀。
更新日期:2020-07-22
中文翻译:
昆虫线粒体作为冷冻诱导损伤的靶点
许多昆虫在内部冷冻中存活下来,但冷冻应激的巨大复杂性阻碍了对冷冻诱导损伤的最终性质的理解。在这里,我们使用果蝇幼虫 Chymomyza costata 来评估线粒体对冷冻应激反应的作用。呼吸分析显示,冷冻敏感(非滞育)表型的脂肪体线粒体在致死性冷冻应激下显着降低耗氧量,而耐冻(滞育、冷驯化)表型的线粒体在相同情况下不会失去呼吸能力。压力。使用透射电子显微镜,我们显示脂肪体和后肠线粒体在冷冻敏感表型暴露于致命的冷冻应激时膨胀,偶尔会破裂。相比之下,在暴露于相同压力的耐冻表型中未观察到线粒体肿胀。我们假设线粒体肿胀是由线粒体内膜的通透性转变及其屏障功能丧失引起的,这导致细胞溶质水渗透流入基质。因此,我们认为向滞育和冷驯化的表型转变可能与适应性变化有关,包括保护线粒体内膜免受通透性转变和随后的线粒体肿胀。高浓度脯氨酸和其他冷冻保护物质的积累可能是这种适应性变化的一部分,因为我们已经表明,通过在脯氨酸增强饮食中喂养冷冻敏感表型幼虫,可以消除冷冻诱导的线粒体肿胀。