Mitochondrial pathway leading to programmed cell death induced by aluminum phytotoxicity in Arabidopsis

Recent studies have reported some apoptosis-like characters under Al treatment including nucleus morphology changes and appearance of nucleus fragmentation in plant cells. Our recent report has suggested that mitochondrial oxidative burst, mitochondrial swelling and mitochondrial transmembrane potential (MTP) disrupt play crucial roles in Al-induced caspase-3-like activation and programmed cell death (PCD). And Complex I and III might be the sources of Al-induced mitochondrial reactive oxygen species (ROS) through interaction between Al and iron-sulfur (Fe-S) protein. Our study contributed to the understanding of mitochondria-dependent cellular signaling cascade of plant biological responses in Al-induced PCD. However, the mitochondria-dependent mechanism in Al-induced PCD needs further improvement, and the roles of mitochondria functional proteins are still poorly understood compared with the study of signaling pathways involved in animal cell apoptosis. By using the fluorescence techniques and the Arabidopsis mesophyll protoplasts as a reference model, the subsequent researches have been carried out to obtain comprehensive understanding of Al-induced plant PCD.