Insect fat body cell morphology and response to cold stress is modulated by acclimation
Insect fat body cell morphology and response to cold stress is modulated by acclimation
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DOI：
10.1242/jeb.189647
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发表时间：
2018-11-01
影响因子：
2.8
通讯作者：
Kostal, Vladimir
中科院分区：
文献类型：
--
作者：
Des Marteaux, Lauren E.;Stetina, Tomas;Kostal, Vladimir
目前对细胞冷冻损伤的本质以及一些动物在冷冻后存活而另一些动物不能存活的机制缺乏机械上的了解。在这里，我们利用可广泛操纵的麦芽蝇幼虫的耐冻性来揭示与冷冻死亡率相关的细胞和组织形态变化。滞育诱导、冷驯化和饲料中补充脯氨酸产生了从弱耐寒到极耐寒的各种麦芽苍蝇。使用共聚焦显微镜和免疫组织化学染色的脂肪体，马氏管和中肠前部，我们描述了这些变异体在暴露于不同的冷应激(从-5摄氏度的寒冷到-196摄氏度的极端冻结)以及从冷暴露中恢复后的组织和细胞骨架(F-肌动蛋白和α-微管蛋白)的形态。脂肪组织似乎对冷冻损伤最敏感：冷冻导致脂滴聚集，α-微管蛋白结构丢失，F-肌动蛋白明显聚集。滞育和冷驯化的结合大大降低了发生这些形态破坏的温度。从冰冻挑战中恢复的幼虫修复了F-肌动蛋白聚集，但不修复脂滴聚合或α-微管蛋白结构。我们的观察表明，脂质聚集和对α-微管蛋白的损伤是冷冻损伤的非致命性形式，并提示肌动蛋白蛋白的修复或移除(而不是保护)是获得性冷冻耐受的潜在机制。
Mechanistic understanding about the nature of cellular cryoinjury and mechanisms by which some animals survive freezing while others do not is currently lacking. Here, we exploited the broadly manipulable freeze tolerance of larval malt flies (Chymomyza costata) to uncover cell and tissue morphological changes associated with freeze mortality. Diapause induction, cold acclimation and dietary proline supplementation generate malt fly variants ranging from weakly to extremely freeze tolerant. Using confocal microscopy and immunostaining of the fat body, Malpighian tubules and anterior midgut, we described tissue and cytoskeletal (F-actin and alpha-tubulin) morphologies among these variants after exposure to various cold stresses (from chilling at -5 degrees C to extreme freezing at -196 degrees C), and upon recovery from cold exposure. Fat body tissue appeared to be the most susceptible to cryoinjury: freezing caused coalescence of lipid droplets, loss of a-tubulin structure and apparent aggregation of F-actin. A combination of diapause and cold acclimation substantially lowered the temperature at which these morphological disruptions occurred. Larvae that recovered from a freezing challenge repaired F-actin aggregation but not lipid droplet coalescence or alpha-tubulin structure. Our observations indicate that lipid coalescence and damage to alpha-tubulin are non-lethal forms of freeze injury, and suggest that repair or removal (rather than protection) of actin proteins is a potential mechanism of acquired freeze tolerance.