Consequences of anthropogenic carbon emissions are warming warming seawater worldwide, pushing the limits of tolerance for corals and driving a decline in biodiversity. The Mediterranean Sea is a climate change hotspot where temperature impacts are very pronounced and have been well-documented across the region over the last 30 years. To determine the influence of warmer conditions on the immune activities of temperate corals, several experimental designs were implemented in both the laboratory and the field, using a wide variety of functional and histological techniques as well as antibodies towards specific molecular targets. The findings of experiments carried out in the laboratory confirmed the regulation of the TLR-NF-kB pathway in colonies of Astroides calycularis under bacterial challenge at control temperature, as well as the interplay of HSP70 in coral responses. Under warmer conditions plus pathogen elicitation, TLR4‑NF‑kB activation was almost completely suppressed, while an upregulation of HSP70 appeared in both treatments at elevated temperature. Results from laboratory and field experiments revealed that several immune-related enzymes (phenoloxidase, glutathione peroxidase, lysozyme, alkaline phosphatase, and esterase) are involved in the responses of A. calycularis, Cladocora caespitosa and Balanophyllia europaea corals to pathogen elicitation and physical injury. However, all species considered showed a strong response alteration (in almost all immune parameters) with thermal stress, indicating a general trend of enhanced effects on constitutive activities but a suppressive impact on injury and/or bacterial challenge. Microbiological analyses from in situ experiments also revealed a shift in the coral-associated bacterial community during the summer period towards pathogen taxa after injuries. These species have the ability to acquire and maintain warming tolerance through stress memory. This is a phenomenon wherein a transient "priming" stimulus leads to a modified and often enhanced response to a subsequent "triggering" stress exposure. The results on C. caespitosa indicated a durable thermal-protective effect in temperate corals due to stress memory, which significantly improved immune tolerance and a bleaching resistance for next 75 days after the priming exposure. Additionally, a significant relationship was found between genomic methylation levels and accumulated thermal stress in corals, preliminarily suggesting an epigenetic regulation dynamic of coral stress tolerance in response to climate change. Such an approach was useful for discovering the impacts of climate change and its effects on the survival chances of temperate corals, combining new immunological information with physiological natural history to better understand what drives the health and resistance of endangered corals.
(2024). IMMUNITY AND TEMPERATE CORAL CRISIS: A NOVEL APPROACH TO DISCOVER IMPACTS AND RESILIENCE UNDER CLIMATE CHANGE SCENARIOS.
IMMUNITY AND TEMPERATE CORAL CRISIS: A NOVEL APPROACH TO DISCOVER IMPACTS AND RESILIENCE UNDER CLIMATE CHANGE SCENARIOS
BISANTI, LUCA
2024-12-16
Abstract
Consequences of anthropogenic carbon emissions are warming warming seawater worldwide, pushing the limits of tolerance for corals and driving a decline in biodiversity. The Mediterranean Sea is a climate change hotspot where temperature impacts are very pronounced and have been well-documented across the region over the last 30 years. To determine the influence of warmer conditions on the immune activities of temperate corals, several experimental designs were implemented in both the laboratory and the field, using a wide variety of functional and histological techniques as well as antibodies towards specific molecular targets. The findings of experiments carried out in the laboratory confirmed the regulation of the TLR-NF-kB pathway in colonies of Astroides calycularis under bacterial challenge at control temperature, as well as the interplay of HSP70 in coral responses. Under warmer conditions plus pathogen elicitation, TLR4‑NF‑kB activation was almost completely suppressed, while an upregulation of HSP70 appeared in both treatments at elevated temperature. Results from laboratory and field experiments revealed that several immune-related enzymes (phenoloxidase, glutathione peroxidase, lysozyme, alkaline phosphatase, and esterase) are involved in the responses of A. calycularis, Cladocora caespitosa and Balanophyllia europaea corals to pathogen elicitation and physical injury. However, all species considered showed a strong response alteration (in almost all immune parameters) with thermal stress, indicating a general trend of enhanced effects on constitutive activities but a suppressive impact on injury and/or bacterial challenge. Microbiological analyses from in situ experiments also revealed a shift in the coral-associated bacterial community during the summer period towards pathogen taxa after injuries. These species have the ability to acquire and maintain warming tolerance through stress memory. This is a phenomenon wherein a transient "priming" stimulus leads to a modified and often enhanced response to a subsequent "triggering" stress exposure. The results on C. caespitosa indicated a durable thermal-protective effect in temperate corals due to stress memory, which significantly improved immune tolerance and a bleaching resistance for next 75 days after the priming exposure. Additionally, a significant relationship was found between genomic methylation levels and accumulated thermal stress in corals, preliminarily suggesting an epigenetic regulation dynamic of coral stress tolerance in response to climate change. Such an approach was useful for discovering the impacts of climate change and its effects on the survival chances of temperate corals, combining new immunological information with physiological natural history to better understand what drives the health and resistance of endangered corals.File | Dimensione | Formato | |
---|---|---|---|
Luca Bisanti.pdf
embargo fino al 31/12/2025
Descrizione: Tesi di dottorato
Tipologia:
Tesi di dottorato
Dimensione
17.93 MB
Formato
Adobe PDF
|
17.93 MB | Adobe PDF | Visualizza/Apri Richiedi una copia |
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.