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The clownfish - sea anemone system is a great example of symbiotic mutualism where host «toxicity» does not impact its symbiont partner, although the underlying protection mechanism remains unclear. The regulation of nematocyst discharge in cnidarians involves N-acetylated sugars like sialic acid, that bind chemoreceptors on the tentacles of sea anemones, leading to the release of stings. It has been suggested that clownfish could be deprived of sialic acid on their skin surface, sparing them from being stung and facilitating mutualism with sea anemones. In this study, we sampled the skin mucus of two anemone symbionts, the clownfish Amphiprion akindynos and the juvenile damselfish Dascyllus trimaculatus, as well as two non-symbiotic adult damselfish Pomacentrus moluccensis and P. pavo. The free and total sialic acid content, including its conjugated form, and three other intermediates of this pathway were quantified using a stable isotope dilution mass spectrometry approach. We found significantly higher levels of sialic acid and its precursor in the non-symbiotic damselfishes. Concentrations of total sialic acid in anemone symbionts ranged between 13 µM and 16 µM, whereas the non-symbiotic damselfishes ranged between 21 µM and 30 µM. The presence of this metabolite and its precursors, as triggers of nematocyst discharge, in anemone symbionts, suggests that this is not the direct mechanism of protection or that the trigger is concentration dependent. This experiment demonstrates that anemone symbionts are not spared by nematocysts because of a lack of N-acetylated sugars, as previously thought, rather the biochemical mechanisms involving N-acetylated sugars are more complex than just a presence/absence of these molecules., Competing Interests: Declarations. Competing interests: Potential conflicts of interest may be present with one of our collaborators, Prof. Vincent Laudet and Dr. Natacha Roux as they work on the same subject at OIST., (© 2025. The Author(s).)

Coronary artery disease (CAD) remains a leading cause of death worldwide and imposes a substantial socioeconomic burden on healthcare. Improving risk stratification in clinical practice could help to combat this burden. As amino acids are biologically active metabolites whose involvement in CAD remains largely unknown, this study investigated associations between circulating amino acid levels and CAD phenotypes. A high-coverage quantitative liquid chromatography-mass spectrometry approach was applied to acquire the serum amino acids profile of age- and sex-coarsened-matched patients with CAD (n = 46, 66.9 years, 74.7% male) and healthy individuals (n = 120, 67.4 years, 74.7% male) from the COmPLETE study. Multiple linear regressions were performed to investigate associations between amino acid levels and (a) the health status (CAD vs. healthy), (b) the number of affected coronary arteries, or (c) the left ventricular ejection fraction. Regressions were adjusted for age, sex, daily physical activity, sampling, and fasting time. Urea cycle amino acids (ornithine, citrulline, homocitrulline, aspartate, and arginine) were significantly and negatively associated with CAD, the number of affected coronary arteries, and the left ventricular ejection fraction. Lysine, histidine, and the glutamine/glutamate ratio were also significantly and negatively associated with the CAD phenotypes. Overall, patients with CAD displayed lower levels of urea cycle amino acids, highlighting a potential role for urea cycle amino acid profiling in cardiovascular risk stratification.Trial registrationThe study was registered on https://www.clinicaltrials.gov (NCT03986892) on June 5, 2019., (© 2024. The Author(s).)