Salt stress and programmed cell death (PCD): mechanisms of ion-specific signals

Programmed cell death (PCD) is very important for cell differentiation and tissue self-stabilization. PCD can regulate plant adaptability to the environment. Recently, it has been confirmed that PCD occurs in plant responses to various abiotic stresses, such as salt stress, cold stress, flooding, and hypoxia. Affemzeller et al. Reported that PCD was induced by salt, and ion effect activated endonuclease to cause PCD. Under salt stress, using non-damage micro-measurement technology combined with fluorescent staining technology to measure the K +, Na + and Ca2 + flow of the cell, the model below can be established. Na + enters the cell through NSCC, causing membrane depolarization and K + outflow. At this time, [Ca2 +] in the cytoplasm increases, resulting in an increase in ROS levels, and Ca2 + in the cytoplasm activates NADPH oxidase through a positive feedback mechanism. This will cause K + outflow of NSCC channels activated by ROS, reduce intracellular K +, activate cysteine ​​hydrolase and lead to PCD. After treating the cells with sorbitol, it was found that K + in the cytoplasm did not decrease, and the depolarization of the cell membrane was prevented by Zn2 + or La3 +. NaCl-induced PCD does not exist in plants lacking KOR channels (such as Arabidopsis gork mutants), and PCD is endogenous (such as antioxidant enzymes) or exogenous (such as diphenyl iodide, mannitol and other ROS in salt-treated cells) Scavenger) Substance inhibition, plants maintain negative membrane potential (such as higher H + -ATPase activity) and are prone to NaCl-induced PCD. These models provide a very important choice for the prediction of PCD under salt stress, and can clearly recognize the process of salt-induced PCD. Keywords: NSCC, non-selective cation channel; PCD, programmed cell death [programmed cell death] [Reprint please indicate the source] Reference: Sergey Shabala. Journal of Experimental Botany, 2009, 60: 709 -712

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