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Does The Glucocorticoid Stress Response Make Toads More Toxic? An Experimental Study on The Regulation of Bufadienolide Toxin Synthesis. / Üveges, Bálint; Kalina, Csenge ; Szabó, Krisztina et al.
Yn: Integrative Organismal Biology, Cyfrol 5, Rhif 1, obad021, 2023, t. obad021.

Allbwn ymchwil: Cyfraniad at gyfnodolynErthygladolygiad gan gymheiriaid

HarvardHarvard

Üveges, B, Kalina, C, Szabó, K, Móricz, ÁM, Holly, D, Gabor, CR, Hettyey, A & Bókony, V 2023, 'Does The Glucocorticoid Stress Response Make Toads More Toxic? An Experimental Study on The Regulation of Bufadienolide Toxin Synthesis', Integrative Organismal Biology, cyfrol. 5, rhif 1, obad021, tt. obad021. https://doi.org/10.1093/iob/obad021

APA

Üveges, B., Kalina, C., Szabó, K., Móricz, Á. M., Holly, D., Gabor, C. R., Hettyey, A., & Bókony, V. (2023). Does The Glucocorticoid Stress Response Make Toads More Toxic? An Experimental Study on The Regulation of Bufadienolide Toxin Synthesis. Integrative Organismal Biology, 5(1), obad021. Erthygl obad021. https://doi.org/10.1093/iob/obad021

CBE

Üveges B, Kalina C, Szabó K, Móricz ÁM, Holly D, Gabor CR, Hettyey A, Bókony V. 2023. Does The Glucocorticoid Stress Response Make Toads More Toxic? An Experimental Study on The Regulation of Bufadienolide Toxin Synthesis. Integrative Organismal Biology. 5(1):obad021. https://doi.org/10.1093/iob/obad021

MLA

VancouverVancouver

Üveges B, Kalina C, Szabó K, Móricz ÁM, Holly D, Gabor CR et al. Does The Glucocorticoid Stress Response Make Toads More Toxic? An Experimental Study on The Regulation of Bufadienolide Toxin Synthesis. Integrative Organismal Biology. 2023;5(1):obad021. obad021. Epub 2023 Meh 5. doi: 10.1093/iob/obad021

Author

Üveges, Bálint ; Kalina, Csenge ; Szabó, Krisztina et al. / Does The Glucocorticoid Stress Response Make Toads More Toxic? An Experimental Study on The Regulation of Bufadienolide Toxin Synthesis. Yn: Integrative Organismal Biology. 2023 ; Cyfrol 5, Rhif 1. tt. obad021.

RIS

TY - JOUR

T1 - Does The Glucocorticoid Stress Response Make Toads More Toxic? An Experimental Study on The Regulation of Bufadienolide Toxin Synthesis

AU - Üveges, Bálint

AU - Kalina, Csenge

AU - Szabó, Krisztina

AU - Móricz, Ágnes M.

AU - Holly, Dóra

AU - Gabor, Caitlin R.

AU - Hettyey, Attila

AU - Bókony, Veronika

N1 - © The Author(s) 2023. Published by Oxford University Press on behalf of the Society for Integrative and Comparative Biology.

PY - 2023

Y1 - 2023

N2 - 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.

AB - 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.

KW - stress response

KW - poison

KW - phenotypic plasticity

KW - corticosterone

KW - ELISA

KW - HPA axis

U2 - 10.1093/iob/obad021

DO - 10.1093/iob/obad021

M3 - Article

C2 - 37435008

VL - 5

SP - obad021

JO - Integrative Organismal Biology

JF - Integrative Organismal Biology

SN - 2517-4843

IS - 1

M1 - obad021

ER -