A shared mechanism of defense against predators and parasites: chitin regulation and its implications for life-history theory.

A shared mechanism of defense against predators and parasites: chitin regulation and its implications for life-history theory.
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DOI:
10.1002/ece3.766
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发表时间:
2013-12
影响因子:
2.6
通讯作者:
Little, Tom J.
Little, Tom J.
中科院分区:
生物学2区
文献类型:
--
作者:
Beckerman, Andrew P.;de Roij, Job;Dennis, Stuart R.;Little, Tom J.

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对捕食者和寄生虫的防御为适应性表型可塑性提供了很好的例证。尽管对这种诱导防御有大量的了解,但它们在很大程度上是孤立地研究的,这是令人惊讶的,因为捕食和寄生在野外是无处不在的,并且同时起作用。这就提出了一种可能性,即受害者必须权衡捕食与寄生的反应。在这里,我们建议,节肢动物的捕食者和寄生虫的反应通常是基于几丁质合成和降解的内分泌调节。这一提议是令人信服的,因为许多诱导性防御都集中在富含几丁质的结构的时间或空间修饰上。此外,我们展示了甲壳素合成途径如何以甲壳素或肠道甲壳素的分裂结束,以及这种形式的分子调控如何被纳入生活史权衡理论,特别是Y模型。因此,我们的假设跨越了几个生物尺度,以解决Stearns的建议,即“内分泌机制可能被证明只是调节遗传协方差表达的生理机制的冰山一角”。
Defenses against predators and parasites offer excellent illustrations of adaptive phenotypic plasticity. Despite vast knowledge about such induced defenses, they have been studied largely in isolation, which is surprising, given that predation and parasitism are ubiquitous and act simultaneously in the wild. This raises the possibility that victims must trade-off responses to predation versus parasitism. Here, we propose that arthropod responses to predators and parasites will commonly be based on the endocrine regulation of chitin synthesis and degradation. The proposal is compelling because many inducible defenses are centered on temporal or spatial modifications of chitin-rich structures. Moreover, we show how the chitin synthesis pathway ends in a split to carapace or gut chitin, and how this form of molecular regulation can be incorporated into theory on life-history trade-offs, specifically the Y-model. Our hypothesis thus spans several biological scales to address advice from Stearns that “Endocrine mechanisms may prove to be only the tip of an iceberg of physiological mechanisms that modulate the expression of genetic covariance”.
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