Dinoflagellates are a general group of phytoplankton, ubiquitous in aquatic environments. Most dinoflagellates are non-obligate autotrophs, subjected to potential physical and chemical DNA-damaging agents, including UV irradiation, in the euphotic zone. Delay of cell cycles by irradiation, as part of DNA damage responses (DDRs), could potentially lead to growth inhibition, contributing to major errors in the estimation of primary productivity and interpretations of photo-inhibition. Their liquid crystalline chromosomes (LCCs) have large amount of abnormal bases, restricted placement of coding sequences at the chromosomes periphery, and tandem repeat-encoded genes. These chromosome characteristics, their large genome sizes, as well as the lack of architectural nucleosomes, likely contribute to possible differential responses to DNA damage agents. In this study, we sought potential dinoflagellate orthologues of eukaryotic DNA damage repair pathways, and the linking pathway with cell-cycle control in three dinoflagellate species. It appeared that major orthologues in photoreactivation, base excision repair, nucleotide excision repair, mismatch repair, double-strand break repair and homologous recombination repair are well represented in dinoflagellate genomes. Future studies should address possible differential DNA damage responses of dinoflagellates over other planktonic groups, especially in relation to possible shift of life-cycle transitions in responses to UV irradiation. This may have a potential role in the persistence of dinoflagellate red tides with the advent of climatic change.

Dinoflagellates are important aquatic microbes and major harmful algal bloom (HAB) agents that form invasive species through ship ballast transfer. UV‐C installations are recommended for ballast treatments and HAB controls, but there is a lack of knowledge in dinoflagellate responses to UV‐C. We report here dose‐dependent cell cycle delay and viability loss of dinoflagellate cells irradiated with UV‐C, with significant proliferative reduction at 800 Jm−2 doses or higher, but immediate LD50 was in the range of 2400–3200 Jm−2. At higher dosages, some dinoflagellate cells surprisingly survived after days of recovery incubation, and continued viability loss, with samples exhibiting DNA fragmentations per proliferative resumption. Sequential cell cycle postponements, suggesting DNA damages were repaired over one cell cycle, were revealed with flow cytometric analysis and transcriptomic analysis. Over a sustained level of other DNA damage repair pathways, transcript elevation was observed only for several components of base pair repair and mismatch repair. Cumulatively, our findings demonstrated special DNA damage responses in dinoflagellate cells, which we discussed in relation to their unique chromo‐genomic characters, as well as indicating resilience of dinoflagellate cells to UV‐C.