In temperate latitudes, toxic cyanobacteria blooms are commonly formed by Microcystis, a well-known producer of the hepatotoxin, microcystin. One complexity in the study of Microcystis blooms has been the co-existence of toxic and non-toxic strains that are morphologically and microscopically indistinguishable. However, recent molecular advances have facilitated the discrimination between these strains as toxic Microcystis cells possess a suite of microcystin synthetase genes (mcyA - mcyJ), while non-toxic strains do not. I strove to better understand the ecology of these strains by examining the effects of nutrients, temperature, and zooplankton grazing on toxic and non-toxic Microcystis via quantification of the microcystin synthetase gene (mcyD; an indicator of toxic  Microcystis) and the small subunit ribosomal RNA gene, 16S (an indicator of total Microcystis). I found that the molecular quantification of toxic (mcyD-possessing) Microcystis was a better predictor of in situ microcystin levels than total cyanobacteria, total Microcystis, chlorophyll a, or other factors, being significantly correlated with the toxin in every ecosystem studied (n = 5). Regarding the effects of nitrogen (N) and phosphorus (P) on Microcystis blooms, I found that first, Microcystis blooms displayed flexibility with regard to N assimilation being able to utilize both inorganic and organic forms of N. Second, toxic and non-toxic strains were promoted by different forms of nitrogen with nitrate and ammonium stimulating the growth of toxic strains and potentially supporting more toxic blooms. Third, P concentrations played a key role in determining whether toxic or non-toxic strains of Microcystis dominated and thus may also influence the toxicity of blooms. The earth’s temperatures have risen measurably during the past century and are expected to continute to rise through this century. Experimentally enhanced temperatures yielded consistently higher growth rates of toxic Microcystis , but did so for non-toxic Microcystis less frequently. This finding suggested that elevated temperatures may yield more toxic Microcystis cells and/or cells with more mcyD copies per cell, with either scenario potentially yielding more toxic blooms. Concurrent increases in temperature and P concentrations often yielded growth rates for toxic Microcystis cells which exceeded either individual treatment suggesting that future P-loading and climatic warming may additively promote toxic Microcystis blooms. Furthermore, my research showed that natural populations of microzooplankton and mesozooplankton were able to graze on both toxic and non-toxic strains of Microcystis with equal success suggesting that the ability to produce microcystin does not provide a defense from grazing. Finally, I observed that natural mesozooplankton communities were able to graze on Microcystis more consistently than cultured mesozooplankton suggesting that zooplankton reared in bloom environments have developed a tolerance to these toxic cyanobacteria. In summary, this dissertation has provided significant new insight into the ecology of toxic and non-toxic strains of the harmful cyanobacterium Microcystis .