Insect capa neuropeptides impact desiccation and cold tolerance
Insect capa neuropeptides impact desiccation and cold tolerance
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DOI：
10.1073/pnas.1501518112
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发表时间：
2015-02
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影响因子：
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通讯作者：
Selim Terhzaz;N. Teets;P. Cabrero;Louise Henderson;M. Ritchie;R. Nachman;J. Dow;D. Denlinger;S. Davies
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作者：
Selim Terhzaz;N. Teets;P. Cabrero;Louise Henderson;M. Ritchie;R. Nachman;J. Dow;D. Denlinger;S. Davies
昆虫是地球上最强壮的生物之一，几乎可以在所有环境中生存，并能够克服包括干燥和寒冷在内的一系列环境压力。尽管干燥和耐寒有许多共同的特征，但这种相关反应的潜在机制尚不清楚。在这里，我们发现一种昆虫神经肽基因与黑腹果蝇对干燥和寒冷的耐受性有关，这表明肾小管上皮中存在一种新机制，可以提高干燥和寒冷的存活率。此外，我们可以利用合理设计的肽模拟类似物逆转rnai诱导的完整果蝇的应激耐受性表型。因此，我们证明了干预由神经肽控制的生理过程的力量，具有控制害虫的潜力。昆虫的成功与它们对环境压力令人印象深刻的耐受性有关，但人们对神经内分泌系统如何调节这种反应知之甚少。本研究表明，能力（capa）神经肽基因是多种双翅目动物的干燥和冷应激反应基因。通过靶向体内基因沉默、生理操作、应激耐受性测试和合理设计的神经肽类似物，我们证明了黑腹果蝇capa神经肽基因及其编码肽改变了干燥和耐寒性。capa基因的敲低增加了干燥耐受性，但延长了冷昏迷恢复时间，注射capa肽类似物可以逆转这两种表型。免疫组织化学染色表明，在干燥和非致死性冷应激期间，capa在表达capa的Va神经元中积累，但直到从每次应激中恢复后才释放。我们的研究结果还表明，由capa肽信号介导的马尔比氏（肾）小管细胞离子和水分稳态调节是昆虫从干燥和冷胁迫中恢复的关键生理机制。这项工作增强了我们对神经内分泌信号如何介导应激耐受性的理解，并说明了合理设计肽类似物作为破坏保护性应激耐受性的药物的使用。
Significance Insects are among the most robust organisms on the planet, surviving in virtually all environments and capable of surmounting a range of environmental stresses including desiccation and cold. Although desiccation and cold tolerance share many common traits, potential mechanisms for such linked responses remain unclear. Here we show that an insect neuropeptide gene is associated with tolerance of both desiccation and cold in Drosophila melanogaster, suggesting a novel mechanism in renal tubule epithelia that enhances survival of both desiccation and cold. Also, we can reverse RNAi-induced stress tolerance phenotypes in intact flies using rationally designed peptide mimetic analogs. We thus demonstrate the power of intervention in physiological processes controlled by neuropeptides, with potential for insect pest control. The success of insects is linked to their impressive tolerance to environmental stress, but little is known about how such responses are mediated by the neuroendocrine system. Here we show that the capability (capa) neuropeptide gene is a desiccation- and cold stress-responsive gene in diverse dipteran species. Using targeted in vivo gene silencing, physiological manipulations, stress-tolerance assays, and rationally designed neuropeptide analogs, we demonstrate that the Drosophila melanogaster capa neuropeptide gene and its encoded peptides alter desiccation and cold tolerance. Knockdown of the capa gene increases desiccation tolerance but lengthens chill coma recovery time, and injection of capa peptide analogs can reverse both phenotypes. Immunohistochemical staining suggests that capa accumulates in the capa-expressing Va neurons during desiccation and nonlethal cold stress but is not released until recovery from each stress. Our results also suggest that regulation of cellular ion and water homeostasis mediated by capa peptide signaling in the insect Malpighian (renal) tubules is a key physiological mechanism during recovery from desiccation and cold stress. This work augments our understanding of how stress tolerance is mediated by neuroendocrine signaling and illustrates the use of rationally designed peptide analogs as agents for disrupting protective stress tolerance.