Cyanobacterial VOCs β-ionone and β-cyclocitral poisoning Lemna turionifera by triggering programmed cell death

β-Ionone and β-cyclocitral are two typical components in cyanobacterial volatiles, which can poison aquatic plants and even cause death. To reveal the toxic mechanisms of the two compounds on aquatic plants through programmed cell death (PCD), the photosynthetic capacities, caspase-3-like activity, DNA fragmentation and ladders, as well as expression of the genes associated with PCD in Lemna turionifera were investigated in exposure to β-ionone (0.2 mM) and β-cyclocitral (0.4 mM) at lethal concentration. With prolonging the treatment time, L. turionifera fronds gradually died, and photosynthetic capacities gradually reduced and even disappeared at the 96th h. This demonstrated that the death process might be a PCD rather than a necrosis, due to the gradual loss of physiological activities. When L. turionifera underwent the death, caspase-3-like was activated after 3 h, and reached to the strongest activity at the 24th h. TUNEL-positive nuclei were detected after 12 h, and appeared in large numbers at the 48th h. The DNA was cleaved by Ca2+-dependent endonucleases and showed obviously ladders. In addition, the expression of 5 genes (TSPO, ERN1, CTSB, CYC, and ATR) positively related with PCD initiation was up-regulated, while the expression of 2 genes (RRM2 and TUBA) negatively related with PCD initiation was down-regulated. Therefore, β-ionone and β-cyclocitral can poison L. turionifera by adjusting related gene expression to trigger PCD. [Display omitted] •β-Ionone and β-cyclocitral killed L. turionifera with physiology gradually losing.•Caspase-3-like was activated during the death, and TUNEL-positive nuclei were found.•DNA showed laddering, which was cleaved by Ca2+-dependent endonucleases.•Expression of 7 genes related with PCD was adjusted to initiate L. turionifera death.