Üveges B, Kalina C, Szabó K, Móricz Á M, Holly D, Gabor C R, Hettyey A, Bókony V
Department of Evolutionary Ecology, Plant Protection Institute, Centre for Agricultural Research, Eötvös Loránd Research Network, Herman Ottó út 15, 1022 Budapest, Hungary.
Molecular Ecology and Evolution at Bangor, School of Natural Sciences, Bangor University, Environment Centre Wales, Bangor LL57 2UW, UK.
Integr Org Biol. 2023 Jun 5;5(1):obad021. doi: 10.1093/iob/obad021. eCollection 2023.
Chemical defense is a crucial component of fitness in many organisms, yet the physiological regulation of defensive toxin synthesis is poorly understood, especially in vertebrates. Bufadienolides, the main defensive compounds of toads, are toxic to many predators and other natural enemies, and their synthesis can be upregulated by stressors, including predation risk, high conspecific density, and pollutants. Thus, higher toxin content may be the consequence of a general endocrine stress response in toads. Therefore, we hypothesized that bufadienolide synthesis may be stimulated by elevated levels of corticosterone (CORT), the main glucocorticoid hormone of amphibians, or by upstream regulators that stimulate CORT production. To test these alternatives, we treated common toad tadpoles with exogenous CORT (exoCORT) or metyrapone (MTP, a CORT-synthesis inhibitor that stimulates upstream regulators of CORT by negative feedback) in the presence or absence of predation cues for 2 or 6 days, and subsequently measured their CORT release rates and bufadienolide content. We found that CORT release rates were elevated by exoCORT, and to a lesser extent also by MTP, regardless of treatment length. Bufadienolide content was significantly decreased by treatment with exoCORT for 6 days but was unaffected by exposure to exoCORT for 2 days or to MTP for either 6 or 2 days. The presence or absence of predation cues affected neither CORT release rate nor bufadienolide content. Our results suggest that changes in bufadienolide synthesis in response to environmental challenges are not driven by CORT but may rather be regulated by upstream hormones of the stress response.
化学防御是许多生物体适应性的关键组成部分，然而，防御性毒素合成的生理调节机制却鲜为人知，尤其是在脊椎动物中。蟾蜍的主要防御化合物蟾蜍二烯羟酸内酯对许多捕食者和其他天敌有毒，其合成可被应激源上调，包括捕食风险、高同种密度和污染物。因此，较高的毒素含量可能是蟾蜍普遍内分泌应激反应的结果。因此，我们假设蟾蜍二烯羟酸内酯的合成可能受到两栖动物主要糖皮质激素皮质酮（CORT）水平升高的刺激，或者受到刺激CORT产生的上游调节因子的刺激。为了测试这些可能性，我们在有或没有捕食线索的情况下，用外源性CORT（exoCORT）或美替拉酮（MTP，一种通过负反馈刺激CORT上游调节因子的CORT合成抑制剂）处理普通蟾蜍蝌蚪2天或6天，随后测量它们的CORT释放率和蟾蜍二烯羟酸内酯含量。我们发现，无论处理时间长短，exoCORT都会提高CORT释放率，MTP在较小程度上也会提高。用exoCORT处理6天可显著降低蟾蜍二烯羟酸内酯含量，但暴露于exoCORT 2天或MTP 6天或2天都不会影响其含量。捕食线索的存在与否既不影响CORT释放率，也不影响蟾蜍二烯羟酸内酯含量。我们的结果表明，蟾蜍二烯羟酸内酯合成对环境挑战的变化不是由CORT驱动的，而是可能由应激反应的上游激素调节的。
