Elevated pCO2 causes a shift towards more toxic microcystin variants in nitrogen-limited Microcystis aeruginosa

Elevated pCO(2) may promote phytoplankton growth, and potentially alleviate carbon limitation during dense blooms. Under nitrogen-limited conditions, elevated pCO(2) may furthermore alter the phytoplankton carbon-nitrogen (C:N) balance and thereby the synthesis of secondary metabolites, such as cyanobacterial toxins. A common group of these toxins are the microcystins, with variants that differ not only in C: N stoichiometry, but also in toxicity. Here, we hypothesized that elevated pCO(2) will increase the cellular C: N ratios of cyanobacteria, thereby promoting the more toxic microcystin variants with higher C: N ratios. To test this hypothesis, we performed chemostat experiments under nitrogen-limited conditions, exposing three Microcystis aeruginosa strains to two pCO(2) treatments: 400 and 1200 mu atm. Biomass, cellular C: N ratios and total microcystin contents at steady state remained largely unaltered in all three strains. Across strains and treatments, however, cellular microcystin content decreased with increasing cellular C: N ratios, suggesting a general stoichiometric regulation. Furthermore, as predicted, microcystin variants with higher C: N ratios generally increased with elevated pCO(2), while the variant with a low C: N ratio decreased. Thus, elevated pCO(2) under nitrogen-limited conditions may shift the cellular microcystin composition towards the more toxic variants. Such CO2-driven changes may have consequences for the toxicity of Microcystis blooms.