Erythromycin sensitivity across different taxa of marine phytoplankton. A novel approach to sensitivity of microalgae and the evolutionary history of the 23S gene

Erythromycin has been recorded in coastal waters and could pose a severe threat to marine microbial life. Macrolides such as erythromycin may affect microalgae by inhibiting the pathways involved in protein synthesis. Toxicological testing of microalgae has proven to be a useful tool for the risk assessment of a substance affecting phytoplankton. Due to the controversial results concerning the sensitivity of microalgal species to erythromycin found in the literature, the goals of this work were, initially, to assess the erythromycin sensitivity of different species of marine microalgae from different and representative taxonomic groups; and, secondly, to examine whether the sensitivity to erythromycin could be explained by the differences in the phylogenetic evolution. We chose eight species: two green algae, four heterokonts, one haptophyte and one dinoflagellate, which were then exposed to erythromycin (0.1 to 10 mg L^-1). Our results showed a wide range of sensitivities indicating that the biology of each species was primarily responsible for the variation observed. To test the second objective, we contrasted different ecotoxicological endpoints (growth, cellular properties and status of the photosynthetic apparatus) with the phylogenetic distribution [eukaryotic host (concatenated nuclear tree), evolutionary history of the chloroplast (16S tree), efficiency and repair of photosystem II (psbA tree), and the binding site of erythromycin (23S tree)] of the species. We found that the growth inhibition of microalgae as a toxicological endpoint was the endpoint best explained by the topology of the 23S rRNA gene tree when it was modelled following a non-stationary evolutionary process.