Signaling Pathways of Aluminum-Induced Programmed Cell Death in Higher Plants

Abstract

Aluminum (Al) is the most abundant metals in the earth’s crust. Al stress triggers the production of nitric oxide (NO) and hydrogen peroxide (H2O2). The homeostasis between NO and H2O2 may be a key decision point of cell survival or cell death. Al toxicity can break NO and H2O2 homeostasis and induce programmed cell death (PCD) in plants, which is characterized by nucleus condensation and crescent-shaped, marginalized chromatin aggregation, and DNA Ladder. This multiple programming and damaged process is mediated via two signaling pathways. One is mitochondria-dependent pathway. The excess Al toxicity-generated production of ROS leads to lipid peroxidation and induces the opening of MPTP, and then causes the release of Cyt c and finally results in PCD. Another is multi-organelle and nucleus-guided mitochondria-independent pathway, which is executed by regulating gene expressions of PCD promoter and suppressor. The promoters include senescence-associated gene (SAG), vacuole processing enzyme (VPE), poly (ADP ribose) polymerase (PARP-1), and PDCD5. Bax inhibitor-1 (BI-1), ACCELERATED CELL DEATH2 (ACD2), and LESION SIMULATING DISEASE1 (LSD1) all belong to the suppressor. There is a negative relationship between the occurrence of PCD and Al resistance, so the negative regulation of Al-induced PCD may be an important mechanism of Al tolerance. In this review, we highlight the newest advances about Al-induced PCD in the context of the relevant literature and enlarge our knowledge on cell death signaling pathways in plants under Al stress.