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Antifouling-induced transcriptional changes in the adhesive pedal disc of Diadumene lineata
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Marine biofouling by sessile invertebrates such as Diadumene lineata poses a persistent threat to marine infrastructure, and antifouling agents are critical for mitigating this issue, yet their molecular mechanisms of action on fouling cnidarians remain poorly understood. In this study, acute toxicity tests and 24 h attachment inhibition assays were conducted, followed by transcriptomic sequencing of pedal disc tissue from D. lineata exposed to N-oleyl-1,3-propanediamine. The 96 h-LC₅₀ of the agent was determined to be 38.66 mg/L, and exposure to 70 mg/L agent achieved complete 24 h attachment inhibition. Transcriptomic analysis identified extensive transcriptional perturbations across four core physiological systems: metabolic reprogramming via activated PPAR signaling, immune dysregulation characterized by impaired antigen processing and DAMP-mediated inflammation, disrupted post-transcriptional regulation and proteostasis, and compromised axon regeneration with decoupled damage sensing and repair. Collectively, these interconnected disruptions synergistically impaired the structural integrity, energy supply, and stress adaptation capacity of pedal disc cells, ultimately leading to adhesion inhibition in D. lineata. This study clarifies the multi-pathway toxic mechanism of antifouling agents in fouling sea anemones, providing a foundational molecular framework for future research.
Title: Antifouling-induced transcriptional changes in the adhesive pedal disc of Diadumene lineata
Description:
Marine biofouling by sessile invertebrates such as Diadumene lineata poses a persistent threat to marine infrastructure, and antifouling agents are critical for mitigating this issue, yet their molecular mechanisms of action on fouling cnidarians remain poorly understood.
In this study, acute toxicity tests and 24 h attachment inhibition assays were conducted, followed by transcriptomic sequencing of pedal disc tissue from D.
lineata exposed to N-oleyl-1,3-propanediamine.
The 96 h-LC₅₀ of the agent was determined to be 38.
66 mg/L, and exposure to 70 mg/L agent achieved complete 24 h attachment inhibition.
Transcriptomic analysis identified extensive transcriptional perturbations across four core physiological systems: metabolic reprogramming via activated PPAR signaling, immune dysregulation characterized by impaired antigen processing and DAMP-mediated inflammation, disrupted post-transcriptional regulation and proteostasis, and compromised axon regeneration with decoupled damage sensing and repair.
Collectively, these interconnected disruptions synergistically impaired the structural integrity, energy supply, and stress adaptation capacity of pedal disc cells, ultimately leading to adhesion inhibition in D.
lineata.
This study clarifies the multi-pathway toxic mechanism of antifouling agents in fouling sea anemones, providing a foundational molecular framework for future research.
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