Although the cyanobacterial toxin microcystin has been detected in Canadian fresh waters, little is known about its prevalence on a national scale. Here, we report for the first time on microcystin in 246 water bodies across Canada based on 3474 analyses. Over the last 10 years, microcystins were detected in every province, often exceeding maximum guidelines for potable and recreational water quality. Microcystins were virtually absent from unproductive systems and were increasingly common in nutrient-rich waters. The probable risk of microcystin concentrations exceeding water quality guidelines was greatest when the ratio of nitrogen (N) to phosphorus (P) was low and rapidly decreased at higher N:P ratios. Maximum concentrations of microcystins occurred in hypereutrophic lakes at mass ratios of N:P below 23. Our models may prove to be useful screening tools for identifying potentially toxic “hotspots” or “hot times” of unacceptable microcystin levels. A future scientific challenge will be to determine whether there is any causal link between N:P ratios and microcystin concentrations, as this may have important implications for the management of eutrophied lakes and reservoirs.

Microcystin is a common and well-known cyanobacterial toxin whose intracellular role is still under investigation. Increasing knowledge on microcystin gene expression and regulation can contribute to the understanding of its putative cellular function. In this work, reverse transcription-quantitative PCR (RT-qPCR) was used to investigate the transcriptional response of the mcyD gene to nitrogen (nitrate and ammonium) and phosphorus limitation in two toxic Microcystis strains. The existence of a direct correlation between transcripts of mcyD and ntcA genes was also identified. In previous studies, NtcA (global nitrogen regulator) has been described as a potential component in the control of microcystin biosynthesis. This research showed that stress agents linked to nutrient deprivation could lead to a significant increase of microcystin production in both strains studied. The more toxic strain proved to be more resistant to nutrient limitation. The similar outcomes of mcyD regulation observed for all nutrients suggest that this response can be linked to oxidative stress of cells undergoing adverse growth conditions.