Aluminum induces rapidly mitochondria-dependent programmed cell death in Al-sensitive peanut root tips

摘要

Background Although many studies suggested that aluminum (Al) induced programmed cell death (PCD) in plants, the mechanism of Al-induced PCD and its effects in Al tolerance is limited. This study was to investigate the mechanism and type of Al induced PCD and the relationship between PCD and Al tolerance. Results In this study, two genotypes of peanut 99–1507 (Al tolerant) and ZH2 (Al sensitive) were used to investigate Al-induced PCD. Peanut root growth inhibition induced by AlCl₃ was concentration and time-dependent in two peanut varieties. AlCl₃ at 100?μM could induce rapidly peanut root tip PCD involved in DNA cleavage, typical apoptotic chromatin condensation staining with DAPI, apoptosis related gene Hrs203j expression and cytochrome C (Cyt c ) release from mitochondria to cytosol. Caspase3-like protease was activated by Al; it was higher in ZH2 than in 99–1507. Al increased the opening of mitochondrial permeability transition pore (MPTP), decreased inner membrane potential (ΔΨ_m) of mitochondria. Compared with the control, Al stress increased O₂ ?- and H₂O₂ production in mitochondria. Reactive oxygen species (ROS) burst was produced at Al treatment for 4?h. Conclusions Al-induced PCD is earlier and faster in Al-sensitive peanut cultivar than in Al-tolerant cultivar. There is a negative relationship between PCD and Al resistance. Mitochondria- dependence PCD was induced by Al and ROS was involved in this process. The mechanism can be explained by the model of acceleration of senescence under Al stress.