β-cyclocitral induced rapid cell death of Microcystis aeruginosa

In this study, M. aeruginosa was exposed to 0-300 mg/L BCC, and the physiological responses were comprehensively studied at the cellular, molecular, and transcriptomic levels. The result indicated that the lethal effect was concentration-dependent; 100 mg/L BCC only caused recoverable stress, while 150-300 mg/L BCC caused rapid rupture of cyanobacterial cells. Scanning electron microscope images suggested two typical morphological changes exposed to above 150 mg/LBCC: wrinkled/shrank with limited holes on the surface at 150 and 200 mg/L BCC exposure; no apparent shrinkage at the surface but with cell perforation at 250 and 300 mg/L BCC exposure. BCC can rapidly inhibit the photosynthetic activity of M. aeruginosa cells (40%∼100% decreases for 100-300 mg/L BCC) and significantly down-regulate photosynthetic system Ⅰ-related genes. Also, chlorophyll a (by 30%∼90%) and ATP (by ∼80%) contents severely decreased, suggesting overwhelming pressure on the energy metabolism in cells. Glutathione levels increased significantly, and stress response-related genes were upregulated, indicating the perturbation of intracellular redox homeostasis. Two cell death pathways were proposed to explain the lethal effect: apoptosis-like death as revealed by the upregulation of SOS response genes when exposed to 200 mg/L BCC and mazEF-mediated death as revealed by the upregulation of mazEF system genes when exposed to 300 mg/L BCC. Results of the current work not only provide insights into th...
Source: Environmental Pollution - Category: Environmental Health Authors: Source Type: research