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Reveillon, D.

Publications and source records attributed to Reveillon, D..

3 recordsLinked to original sources

Paralytic Shellfish Toxin production in Alexandrium minutum (Dinophyceae): insights from omics integration using toxigenic and non-toxigenic recombinant progeny

Paralytic Shellfish Toxins (PSTs) are produced by certain species of cyanobacteria and dinoflagellates. Part of the PST biosynthetic pathway has been elucidated in cyanobacteria, and the implication of some sxt genes has been confirmed by experimental studies. Contrary to cyanobacteria, knowledge about PST biosynthesis in dinoflagellates is more limited and generally restricted to comparative studies with the cyanobacterial pathway. To investigate the specificity of the PST pathway in dinoflagellates, 16 toxic and non-toxic A. minutum strains from a recombinant cross were compared, without prior assumption on genes or metabolites involved in PST synthesis, using an integrative approach combining untargeted metabolomic and transcriptomic data. Among the 60 most distinguishing transcripts between toxic and non-toxic strains, only 3 sxt genes were present, sxtA4, sxtG, and sxtI. In contrast, non-sxt homologs were detected as highly discriminant between these two phenotypes. More specifically, a phyH homolog may act as the analog of sxtS found in cyanobacteria. Moreover, we identified four putative synthetic PST intermediates. Among these, Int-C2, correlated with the toxic phenotype, whereas 3 others were detected in both toxic and non-toxic strains, suggesting that these strains may share some parts of the biosynthetic pathway. Finally, our results showed that PST biosynthesis in dinoflagellate results from the activity of sxt genes, acquired by horizontal gene transfer from cyanobacteria, as well as from other genes not acquired from cyanobacteria, such as phyH.

genomics↗

Multi-omics uncovers nutrient stress-driven interactions in the Prymnesium parvum holobiont, with vitamin B12 limitation highlighting mutualism.

Microalgal-bacterial interactions are central to nutrient cycling and ecosystem functioning in marine habitats, yet the mechanisms structuring these associations under defined nutrient constraints remain poorly resolved. Using a synthetic 15-member bacterial community (SynCom) and controlled nitrogen (N), phosphorus (P), and vitamin B12 limitation, we investigated how nutrient scarcity shapes the physiology, metabolism, and transcriptional activity of the harmful alga Prymnesium parvum and its associated microbiota. Under N- and P-limitation, the SynCom had minimal impact on algal growth despite nutrient-dependent shifts in toxin production and metabolite profiles. In contrast, B12-limitation triggered a strong mutualistic interaction in which the SynCom enabled a three-fold increase in algal biomass and drove restructuring of intracellular and extracellular metabolomes, including the accumulation of ectoine and membrane-associated lipids and the depletion of thiamine-like and stress-associated metabolites. Metabarcoding revealed stable community composition but enrichment of B12-producing taxa under B12-limited conditions, while metatranscriptomics uncovered functional divergence among SynCom members. Bacteria segregated into specialized B12- or N-responsive strains and metabolically plastic generalists sustaining broad transcriptional activity across all nutrient regimes. B12 producers (Marinovum algicola, Roseobacter sp., Halomonas sp.) upregulated cobalamin biosynthesis exclusively under B12 limitation, whereas several dependent taxa induced B12 transport and B12-requiring enzymes, indicating active vitamin exchange within the holobiont. P. parvum displayed nutrient-specific transcriptional programs, with B12-limited co-cultures shifting toward growth-associated gene expression despite constitutive expression of the B12-dependent metH gene. These results demonstrate that vitamin auxotrophy acts as a key metabolic lever reorganizing holobiont function, driving reciprocal benefits and reprogramming algal-bacterial metabolism in our synthetic system.

microbiology↗

Effects of copepod chemical cues on intra- and extracellular toxins in two species of Dinophysis

Copepods may contribute to harmful algal bloom formation by selectively rejecting harmful cells. Additionally, copepods and the chemical cues they exude, copepodamides, have been shown to induce increased toxin production in paralytic and amnesic toxin producing microalgae. However, it is unknown if diarrhetic shellfish toxin (DST) producers such as Dinophysis respond to copepods or copepodamides in a similar fashion. Here we expose laboratory cultures of Dinophysis sacculus and D. acuminata to direct grazing by Acartia sp. copepods or copepodamides and measure their toxins after three days. Total Dinophysis- produced toxins (DPTs), okadaic acid, pectenotoxin-2, and C9-diol ester of okadaic acid, increased by 8 - 45% in D. sacculus but was significantly different from controls only in the highest (10 nM) copepodamide treatment whereas toxin content was not affected in D. acuminata. Growth rate was low across all groups and explained up to 91% of the variation in toxin content. DPTs were redistributed from internal compartments to the extracellular medium in the highest copepodamide treatments (5 - 10 nM), which were two to three times higher than controls and indicates an active release or passive leakage of toxins. Untargeted analysis of endometabolomes indicated significant changes in metabolite profiles for both species in response to the highest copepodamide treatments, independent of known toxins. However, it is not clear whether these are stress responses or caused by more complex mechanisms. The relatively small grazer-induced effect in Dinophysis observed here, compared to several species of Alexandrium and Pseudo-nitzschia reported previously, suggests that DPT production in Dinophysis is likely not induced by copepods, except perhaps in patches with high copepod densities. Thus, DPTs may, represent either a constitutive chemical defence for Dinophysis, or serve an altogether different purpose.

ecology↗