This review summarizes the present state of knowledge regarding the toxic, bloom-forming cyanobacterium, Microcystis, with a specific focus on its geographic distribution, toxins, genomics, phylogeny, and ecology. A global analysis found documentation suggesting geographic expansion of Microcystis, with recorded blooms in at least 108 countries, 79 of which have also reported the hepatatoxin microcystin. The production of microcystins (originally "Fast-Death Factor") by Microcystis and factors that control synthesis of this toxin are reviewed, as well as the putative ecophysiological roles of this metabolite. Molecular biological analyses have provided significant insight into the ecology and physiology of Microcystis, as well as revealed the highly dynamic, and potentially unstable, nature of its genome. A genetic sequence analysis of 27 Microcystis species, including 15 complete/draft genomes are presented. Using the strictest biological definition of what constitutes a bacterial species, these analyses indicate that all Microcystis species warrant placement into the same species complex since the average nucleotide identity values were above 95%, 16S rRNA nucleotide identity scores exceeded 99%, and DNA-DNA hybridization was consistently greater than 70%. The review further provides evidence from around the globe for the key role that both nitrogen and phosphorus play in controlling Microcystis bloom dynamics, and the effect of elevated temperature on bloom intensification. Finally, highlighted is the ability of Microcystis assemblages to minimize their mortality losses by resisting grazing by zooplankton and bivalves, as well as viral lysis, and discuss factors facilitating assemblage resilience.

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Since the mid-twentieth century, both nutrient delivery rates and the frequency of harmful algal blooms (HABs) in coastal aquatic ecosystems have intensified. Recent studies have shown that nitrogen (N) or phosphorus (P) can limit primary production in freshwater systems, and Microcystis is able to utilize both inorganic and organic forms of N. The present study quantified the microcystin synthetase gene (mcyD) and the ribosomal RNA gene (16S) to assess how various nutrient sources affected the growth of toxic and non-toxic strains of Microcystis during natural blooms. During the present study, dense Microcystis blooms (>10 6 cell equivalents l-1) were observed within 2 contrasting ecosystems in the eastern USA: a tidal tributary and a eutrophic lake. In both systems, all Microcystis populations were stimulated by N more frequently than P during nutrient amendment experiments. The abundance of toxic strains of Microcystis was enhanced by nutrient enrichment more frequently (83% of experiments) than non-toxic strains (58% of experiments), suggesting that toxic strains may have a greater demand for both nutrients. Furthermore, abundances of toxic strains of Microcystis were enhanced by inorganic N more frequently (67% of experiments) than organic N (8% of experiments), while non-toxic strains were stimulated by organic N (50% of experiments) more frequently than inorganic N (25% of experiments). Inorganic P increased abundances of toxic strains of Microcystis more frequently than non-toxic strains (42 and 33% of experiments, respectively). Therefore, the dominance of toxic Microcystis may be influenced by both the concentration and species of nutrients, with higher concentrations of inorganic N and/or P likely promoting blooms dominated by toxic strains and potentially yielding higher microcystin concentrations.

Whole transcriptome shotgun sequencing (RNA-seq) was used to assess the transcriptomic response of the toxic cyanobacterium Microcystis aeruginosa during growth with low levels of dissolved inorganic nitrogen (low N), low levels of dissolved inorganic phosphorus (low P), and in the presence of high levels of high molecular weight dissolved organic matter (HMWDOM). Under low N, one third of the genome was differentially expressed, with significant increases in transcripts observed among genes within the nir operon, urea transport genes (urtBCDE), and amino acid transporters while significant decreases in transcripts were observed in genes related to photosynthesis. There was also a significant decrease in the transcription of the microcystin synthetase gene set under low N and a significant decrease in microcystin content per Microcystis cell demonstrating that N supply influences cellular toxicity. Under low P, 27% of the genome was differentially expressed. The Pho regulon was induced leading to large increases in transcript levels of the alkaline phosphatase phoX, the Pst transport system (pstABC), and the sphX gene, and transcripts of multiple sulfate transporter were also significantly more abundant. While the transcriptional response to growth on HMWDOM was smaller (5–22% of genes differentially expressed), transcripts of multiple genes specifically associated with the transport and degradation of organic compounds were significantly more abundant within HMWDOM treatments and thus may be recruited by Microcystis to utilize these substrates. Collectively, these findings provide a comprehensive understanding of the nutritional physiology of this toxic, bloom-forming cyanobacterium and the role of N in controlling microcystin synthesis.