Nitric Oxide Inhibits Al-Induced Programmed Cell Death in Root Tips of Peanut (Arachis hypogaea L.) by Affecting Physiological Properties of Antioxidants Systems and Cell Wall.

Chun-Liu Pan,Dong Xiao,Ya-Lun Wang,Ai-Qin Wang,Jie Zhan,Wei-Jiao Xiong,Shao-Chang Yao,Shu-Zhen Luo,Long-Fei He

doi:10.3389/fphys.2017.01037

Chun-Liu Pan, Dong Xiao + Show 7 more

Open Access

https://doi.org/10.3389/fphys.2017.01037

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Abstract

It has been reported that nitric oxide (NO) is a negative regulator of aluminum (Al)-induced programmed cell death (PCD) in peanut root tips. However, the inhibiting mechanism of NO on Al-induced PCD is unclear. In order to investigate the mechanism by which NO inhibits Al-induced PCD, the effects of co-treatment Al with the exogenous NO donor or the NO-specific scavenger on peanut root tips, the physiological properties of antioxidants systems and cell wall (CW) in root tip cells of NO inhibiting Al-induced PCD were studied with two peanut cultivars. The results showed that Al exposure induced endogenous NO accumulation, and endogenous NO burst increased antioxidant enzyme activity in response to Al stress. The addition of NO donor sodium nitroprusside (SNP) relieved Al-induced root elongation inhibition, cell death and Al adsorption in CW, as well as oxidative damage and ROS accumulation. Furthermore, co-treatment with the exogenous NO donor decreased MDA content, LOX activity and pectin methylesterase (PME) activity, increased xyloglucan endotransglucosylase (XET) activity and relative expression of the xyloglucan endotransglucosylase/hydrolase (XTH-32) gene. Taken together, exogenous NO alleviated Al-induced PCD by inhibiting Al adsorption in CW, enhancing antioxidant defense and reducing peroxidation of membrane lipids, alleviating the inhibition of Al on root elongation by maintaining the extensibility of CW, decreasing PME activity, and increasing XET activity and relative XTH-32 expression of CW.

Highlights

Aluminum (Al) toxicity is the main reason for large-scale decline of arable land
Our previous studies showed that there was a negative relationship between Programmed cell death (PCD) and Al tolerance, and that the exogenous nitric oxide (NO) donor sodium nitroprusside (SNP) inhibited Al-induced PCD occurrence (Zhan et al, 2013; Huang et al, 2014a,b; He et al, 2017)
SNP and cPTIO alone had no effect on root elongation compared to the control

Summary

Introduction

Aluminum (Al) toxicity is the main reason for large-scale decline of arable land. In acidic soils with pH lower than 4.5, Al becomes the soluble Al3+ ion, released into soil solution and resulting in plant Al stress, which subsequently affects a plant’s ability to take up water and nutrients; as a consequence, Al toxicity is among the most important factors limiting crop growth and productionNO Inhibits Al-Induced PCD (Matsumoto et al, 2015). In acidic soils with pH lower than 4.5, Al becomes the soluble Al3+ ion, released into soil solution and resulting in plant Al stress, which subsequently affects a plant’s ability to take up water and nutrients; as a consequence, Al toxicity is among the most important factors limiting crop growth and production. There is an urgent need to understand the mechanism of Al tolerance in other plants, to help us to solve the problems of food shortage and inadequate biofuel production from acid soils (Sun et al, 2015). Our previous studies showed that there was a negative relationship between PCD and Al tolerance, and that the exogenous nitric oxide (NO) donor sodium nitroprusside (SNP) inhibited Al-induced PCD occurrence (Zhan et al, 2013; Huang et al, 2014a,b; He et al, 2017)

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