Evaluation of the Effects of Different Phosphorus Sources on Microcystis aeruginosa Growth and Microcystin Production via Transcriptomic Surveys

Abstract

Microcystis aeruginosa (M. aeruginosa) is a dominant species among frequent cyanobacterial blooms and is well known for its toxin-producing ability. Phosphorus (P) is a typical growth-limiting element for M. aeruginosa. Although alterations in physiological reactions have been documented in response to various P sources, the underlying molecular processes and transcriptional patterns remain poorly understood. This study evaluated the physiological and molecular responses of M. aeruginosa to different P sources. The growth of M. aeruginosa was promoted by both dissolved inorganic phosphorus (DIP) and dissolved organic phosphorus (DOP) at a concentration of 0.4 mg/L with an initial cell density of 1.50 (±0.05) × 106 cells/mL. The cell density reached 1.38 (±0.05) × 107 cells/mL in the DIP group on day 14, a value which was higher than that in the DOP group. Most photosynthesis genes had higher levels of upregulated expression in the DIP group. For instance, gene psbA was upregulated by 0.45 Log2Fold Change (Log2FC). In the DOP group, it is interesting that the Pi (PO4-P) concentration increased to 0.09 mg/L on day 14. Meanwhile, the expression of the gene encoding alkaline phosphatase-like protein was significantly upregulated, with a value of 1.56 Log2FC, and the alkaline phosphatase concentration increased in the DOP group. The intracellular microcystin (IMC) concentration decreased with time in both groups. However, the concentration of extracellular microcystins (EMCs) increased with incubation time in both groups. Phosphorus participates in the regulation of microcystin synthesis, mainly by regulating ATP synthesis. Based on the physiological and molecular investigations in this study, the results provide crucial insights into the physiological adaptations and the role of P in modulating harmful algal bloom formation, microcystin synthesis, and potential molecular responses of M. aeruginosa.