Response of cytotoxin production ability to gene expression and cell molecular structure of Microcystis aeruginosa FACHB-905

To investigate the inhibitory mechanism of artemisinin sustained-release microspheres (ASMs) on Microcystis aeruginosa (M. aeruginosa) from the molecular level, prx, psbA, fabZ, and mcyD were studied, and the cell death mode were also explored. The results showed that expression of prx was slightly up-regulated, while the expression of psbA, fabZ, and mcyD was significantly reduced. It can infer that oxidant damage and photic damage are the main mechanisms for the algicidal effect of ASMs on M. aeruginosa. It can be seen from the changes in cell morphology and structure that microspheres stress triggers apoptosis-like cell death, and the cell membrane is intact effectively preventing the leakage of microcystin-LR (MC-LR). Moreover, the down-regulation of mcyD gene also played major role in less extracellular MC-LR than intracellular MC-LR. It was concluded that the ASMs will not cause secondary ecological hazards while killing algae cells and have good application prospects.

Automated summary

To investigate the inhibitory mechanism of artemisinin sustained-release microspheres (ASMs) on Microcystis aeruginosa (M. aeruginosa) from the molecular level, the expression of prx, psbA, fabZ, and mcyD genes were studied, and the cell death mode was explored. The results showed that the up-regulation of prx and the down-regulation of psbA, fabZ, and mcyD play a role in the algicidal effect of ASMs on M. aeruginosa. The ASMs trigger apoptosis-like cell death and effectively prevent the leakage of microcystin-LR (MC-LR), making them a promising application for killing algae cells without causing secondary ecological hazards.