Multiomics reprogramming reverses disease susceptibility in Magallana gigas during aging
Abstract
Background: Aging is a progressive and irreversible biological process that typically increases susceptibility to infectious diseases. However, unexpectedly, the opposite outcome was observed in oysters: older oysters exhibit increased tolerance to Pacific oyster mortality syndrome (POMS), a panzootic disease responsible for severe losses worldwide. We investigated this pattern by challenging four biparental families of oysters aged 4, 16, and 28 months. We conducted an integrative multiomics analysis, which included epigenomics, transcriptomics, and metabolomics, on the two families that exhibited the greatest age-related increase in survival. Results: Our results reveal that aging is characterized by coordinated epigenetic, transcriptional, and metabolic reprogramming that reduces host permissiveness to POMS. We show that the epigenetic remodeling of immune regulators (e.g., toll-like receptors and myeloid differentiation primary response 88; MyD88) aligns with the transcriptional rewiring of the nuclear factor-kappa B (NF-κB) and ubiquitin pathways, producing a tuned state with enhanced antiviral activity. We also identify age-related repression of mechanistic target of rapamycin (mTOR) signaling, which likely promotes autophagy and enhances viral control. These changes are tightly linked to metabolic adjustments, including reduced activity of the tricarboxylic acid cycle (TCA), altered nitrogen metabolism, and altered glutathione dynamics, supporting a stress-tolerant, energy-conserving phenotype. Conclusions: Together, our findings reveal juveniles prioritize growth at the cost of viral susceptibility, whereas adults invest in cellular maintenance and antiviral preparedness.
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BibTeX
@article{valdivieso2026multiomics,
title = {{Multiomics reprogramming reverses disease susceptibility in Magallana gigas during aging}},
author = {Alejandro Valdivieso and Leo Duperret and Bruno Petton and Gaelle Courtay and Océane Romatif and Juliette Pouzadoux and Sylvain Henry and Andrei Turtoi and Eve Toulza and Arnaud Lagorce and Lionel Dégremont and Benjamin Morga and Emmanuel Vignal and Celine Cosseau and Fabrice Pernet and Guillaume Mitta and Jeremie Vidal-Dupiol},
journal = {BMC Biology},
year = {2026},
month = sep,
doi = {10.1186/s12915-026-02722-4},
url = {https://hal.science/hal-05786701v1},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Multiomics reprogramming reverses disease susceptibility in Magallana gigas during aging
AU - Alejandro Valdivieso
AU - Leo Duperret
AU - Bruno Petton
AU - Gaelle Courtay
AU - Océane Romatif
AU - Juliette Pouzadoux
AU - Sylvain Henry
AU - Andrei Turtoi
AU - Eve Toulza
AU - Arnaud Lagorce
AU - Lionel Dégremont
AU - Benjamin Morga
AU - Emmanuel Vignal
AU - Celine Cosseau
AU - Fabrice Pernet
AU - Guillaume Mitta
AU - Jeremie Vidal-Dupiol
PY - 2026
DA - 2026/09/04
JO - BMC Biology
DO - 10.1186/s12915-026-02722-4
UR - https://hal.science/hal-05786701v1
AB - Background: Aging is a progressive and irreversible biological process that typically increases susceptibility to infectious diseases. However, unexpectedly, the opposite outcome was observed in oysters: older oysters exhibit increased tolerance to Pacific oyster mortality syndrome (POMS), a panzootic disease responsible for severe losses worldwide. We investigated this pattern by challenging four biparental families of oysters aged 4, 16, and 28 months. We conducted an integrative multiomics analysis, which included epigenomics, transcriptomics, and metabolomics, on the two families that exhibited the greatest age-related increase in survival. Results: Our results reveal that aging is characterized by coordinated epigenetic, transcriptional, and metabolic reprogramming that reduces host permissiveness to POMS. We show that the epigenetic remodeling of immune regulators (e.g., toll-like receptors and myeloid differentiation primary response 88; MyD88) aligns with the transcriptional rewiring of the nuclear factor-kappa B (NF-κB) and ubiquitin pathways, producing a tuned state with enhanced antiviral activity. We also identify age-related repression of mechanistic target of rapamycin (mTOR) signaling, which likely promotes autophagy and enhances viral control. These changes are tightly linked to metabolic adjustments, including reduced activity of the tricarboxylic acid cycle (TCA), altered nitrogen metabolism, and altered glutathione dynamics, supporting a stress-tolerant, energy-conserving phenotype. Conclusions: Together, our findings reveal juveniles prioritize growth at the cost of viral susceptibility, whereas adults invest in cellular maintenance and antiviral preparedness.
SN - 1741-7007
SN - 1741-7007
ER -