ИСТИНА

Marine planktonic dinoflagellates are an ecologically important group of single-cell eukaryotes which show fast reproduction rates, especially in the coastal waters and estuaries, and pronounced physiological adaptability to various types of stress. These protists respond to stress conditions by activation of their defensive mechanisms, which can differ from those of large multicellular forms. The goal of this paper is to demonstrate what cell and molecular mechanisms underpin the fast and effective adaptations of the invasive for the Baltic Sea dinoflagellates Prorocentrum minimum (or P. cordatum), which have recently become good model organisms in the environmental and cell biology studies of unicellular eukaryotes. We focused on cell metabolism and ion channel research, as well as on the effects of different levels of salinity and elevated temperature on cell mortality, cell cycle pattern, RNA synthesis, and DNA replication in P. minimum. It appears that P. minimum can utilize urea as a source of organic nitrogen but also as a source of carbon. Moreover, urea inhibits assimilation of nitrate (the “classic” source of nitrogen) and thus can be the preferable substrate in the coastal waters. Dinoflagellates show elevated biosynthetic activity and low cell-death level at critical salinity 5-8. We infer that this potentially toxic, bloom forming dinoflagellate species displays great colonizing ability across new ecosystems due to high physiological plasticity and pronounced adaptation potential at different levels of biological organization, from molecules and cells to populations. Understanding how unicellular invaders could adapt to harsh environment is of significant importance, especially when this environment represents a large water body which plays a key role in the economy of coastal areas of several densely populated Baltic countries. New molecular data provide better understanding of why protistan diversity peaks in the environment which is adverse for metazoans. Supported by Russian Science Foundation, grant 16-14-10116.