Sodium distribution predicts the chill tolerance of Drosophila melanogaster raised in different thermal conditions
Sodium distribution predicts the chill tolerance of Drosophila melanogaster raised in different thermal conditions
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DOI：
10.1152/ajpregu.00465.2014
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发表时间：
2015-05-15
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影响因子：
--
通讯作者：
Overgaard, Johannes
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文献类型：
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作者：
MacMillan, Heath A.;Andersen, Jonas L.;Overgaard, Johannes
许多昆虫，包括模式全变态昆虫黑腹果蝇（Drosophila melanogaster），在发育期间或作为成虫经历的热环境中表现出显著的耐寒性可塑性。在低温下，许多昆虫失去了调节Na+平衡的能力，这被认为是导致血淋巴水向组织和肠腔的二次损失，其浓缩了血淋巴中剩余的K+。由此产生的细胞外[K+]的增加抑制神经肌肉兴奋性，并提出引起细胞凋亡和损伤。本研究调查是否以及如何变化的耐寒性诱导通过发展和成人冷驯化与Na+，水，和K+平衡的变化。发育期和成株期冷锻炼提高了冬小麦的耐冷性。以添加剂的方式添加黑腹素。与提出的模型一致，这些效应与冷暴露前Na+分布的差异密切相关，例如耐冷苍蝇的血淋巴[Na+]较低，而细胞内[Na+]在处理组之间相似。低血淋巴Na+的冷驯化苍蝇，使他们能够保持血淋巴容量，防止高钾血症，并避免伤害后，慢性冷暴露。这些发现扩展了早期的观察，即在冷暴露于最普遍的模式昆虫（D。melanogaster），强调了发育和成虫热可塑性的共同机制，并为离子调节失败作为昆虫寒冷易感性的中心机制提供了强有力的支持。
Many insects, including the model holometabolous insect Drosophila melanogaster, display remarkable plasticity in chill tolerance in response to the thermal environment experienced during development or as adults. At low temperatures, many insects lose the ability to regulate Na+ balance, which is suggested to cause a secondary loss of hemolymph water to the tissues and gut lumen that concentrates the K+ remaining in the hemolymph. The resultant increase in extracellular [K+] inhibits neuromuscular excitability and is proposed to cause cellular apoptosis and injury. The present study investigates whether and how variation in chill tolerance induced through developmental and adult cold acclimation is associated with changes in Na+, water, and K+ balance. Developmental and adult cold acclimation improved the chilling tolerance of D. melanogaster in an additive manner. In agreement with the proposed model, these effects were intimately related to differences in Na+ distribution prior to cold exposure, such that chill-tolerant flies had low hemolymph [Na+], while intracellular [Na+] was similar among treatment groups. The low hemolymph Na+ of cold-acclimated flies allowed them to maintain hemolymph volume, prevent hyperkalemia, and avoid injury following chronic cold exposure. These findings extend earlier observations of hemolymph volume disruption during cold exposure to the most ubiquitous model insect (D. melanogaster), highlight shared mechanisms of developmental and adult thermal plasticity and provide strong support for ionoregulatory failure as a central mechanism of insect chill susceptibility.