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Epigenomic patterns in fish with divergent cortisol reactivity
Selim Ben Chehida1, Athanasios Samaras2, Madoka V Krick1
1UMR ISEM - CNRS IRD UM EPHE CIRAD, Montpellier, France.
Physiological Genomics
|August 11, 2026
Summary
This study reveals how stress impacts DNA methylation in European seabass, identifying specific epigenetic markers linked to cortisol reactivity. These findings offer potential biomarkers for stress in fish.
Area of Science:
- Endocrinology
- Epigenetics
- Animal Physiology
Background:
- Glucocorticoids (GCs) mediate stress responses and are linked to epigenetic modifications.
- Understanding epigenetic profiles in individuals with varying cortisol reactivity is crucial but understudied.
- Divergent cortisol reactivity influences physiological and behavioral adaptations to stress.
Purpose of the Study:
- To investigate genome-wide DNA methylation differences in European seabass with distinct cortisol reactivity phenotypes.
- To analyze epigenetic changes before and after a chronic stress challenge.
- To identify potential epigenetic biomarkers associated with stress response.
Main Methods:
- Measured cortisol levels in 400 European seabass to identify low- and high-responsiveness phenotypes (n=80).
- Analyzed the methylome at 41,132 CpG sites in blood samples before and after a three-month stress test.
- Assessed physiological parameters including weight, lysozyme activity, glucose, and lactate levels.
Main Results:
- Identified 273 differentially methylated cytosines mapping to 159 differentially methylated genes (DMGs).
- Categorized methylation as 'constitutive' or 'induced' for each phenotype and stress condition.
- Found many DMGs related to GC signaling, with seven showing methylation rewiring (hypo- to hypermethylation).
Conclusions:
- Genome-wide epigenetics can reveal endocrine divergence in stress-responsive phenotypes.
- Identified potential blood-based stress biomarkers in European seabass relevant to cortisol action.
- Highlights the dynamic nature of epigenetic modifications in response to chronic stress.
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