English: The hypothetical conceptual model coupling programmed cell death (PCD) and the role of microcystins (MCs) in Microcystis. (1) The extracellular stressor (e.g., ultraviolet radiation) acts on the cell. (2) Intracellular oxidative stress increases; the intracellular reactive oxygen species (ROS) content exceeds the antioxidative capacity of the cell (mediated mostly by an enzymatic system involving a superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX)) and causes molecular damage. (3) The damage further activates the caspase-like activity, and apoptosis-like death is initiated. Simultaneously, intracellular MCs begin to be released into the extracellular environment. (4) The extracellular MCs have been significantly released from dead Microcystis cells. (5) They act on the remaining Microcystis cells, and exert extracellular roles, for example, extracellular MCs can increase the production of extracellular polysaccharides (EPS) that are involved in colony formation. Eventually, the colonial form improves the survival of the remaining cells under stressful conditions. Source: https://doi.org/10.3390/toxins11120706