No abstract

This work demonstrates a contribution of ethylene and NO (nitric oxide) in MP (mastoparan)-induced cell death in the green algae Chlamydomonas reinhardtii. Following MP treatment, C. reinhardtii showed massive cell death, expressing morphological features of PCD (programmed cell death). A pharmacological approach involving combined treatments with MP and ethylene- and NO-interacting compounds indicated the requirement of trace amounts of both ethylene and NO in MP-induced cell death. By employing a carbon dioxide laser-based photoacoustic detector to measure ethylene and a QCL (quantum cascade laser)-based spectrometer for NO detection, simultaneous increases in the production of both ethylene and NO were observed following MP application. Our results show a tight regulation of the levels of both signalling molecules in which ethylene stimulates NO production and NO stimulates ethylene production. This suggests that, in conjunction with the elicitor, NO and ethylene cooperate and act synchronously in the mediation of MP-induced PCD in C. reinhardtii. To the best of our knowledge, this is the first report on the functional significance of ethylene and NO in MP-induced cell death.

In C. reinhardtii MP triggered PCD of atypical phenotype comprising features of vacuolar and necrotic cell deaths, reminiscent of the modality of hypersensitive response. It was assumed that depending on the physiological state and sensitivity of the cells to MP, the early cell-death phase might be not mediated by caspase-like enzymes, whereas later cell death may involve caspase-like-dependent proteolysis. The findings substantiate the hypothesis that, depending on the mode of induction and sensitivity of the cells, algal PCD may take different forms and proceed through different pathways.

No abstract

Our aim was to investigate the ability of cadmium to induce programmed cell death in tomato suspension cells and to determine the involvement of proteolysis, oxidative stress and ethylene. Tomato suspension cells were exposed to treatments with CdSO(4) and cell death was calculated after fluorescein diacetate staining of the living cells. Ethylene was measured in a flow-through system using a laser-driven photo acoustic detector; hydrogen peroxide was determined by chemiluminescence in a ferricyanide-catalysed oxidation of luminol. We have demonstrated that cadmium induces cell death in tomato suspension cells involving caspase-like proteases, indicating that programmed cell death took place. Using range of inhibitors, we found that cysteine and serine peptidases, oxidative stress, calcium and ethylene are players in the cadmium-induced cell death signaling. Cadmium-induced cell death in tomato suspension cells exhibits morphological and biochemical similarities to plant hypersensitive response and to cadmium effects in animal systems.