Nitric oxide is a suppressor of aluminum-induced mitochondria and caspase-like protease-dependent programmed cell death in plants

Huyi He; Long-Fei He

doi:10.1080/15592324.2019.1640566

Nitric oxide is a suppressor of aluminum-induced mitochondria and caspase-like protease-dependent programmed cell death in plants

Plant Signal Behav. 2019;14(9):1640566. doi: 10.1080/15592324.2019.1640566. Epub 2019 Jul 11.

Authors

Huyi He^{1

2}, Long-Fei He¹

Affiliations

¹ College of Agronomy, Guangxi Key Laboratory for Agro-Environment and Agro-Product Safety, Guangxi University , Nanning , PR China.
² Cash Crops Research Institute, Guangix Academy of Agricultural Sciences , Nanning 530004 , PR China.

Abstract

Aluminum (Al) promotes programmed cell death (PCD) in plants. Although a lot of knowledge about the mechanisms of Al tolerance has been learned, how Al-induced PCD is regulated by nitric oxide (NO) is poorly understood. Mitochondrion is the regulatory center for PCD. We found that Al reduced the level of mitochondrial NO/H₂O₂, promoted the opening of mitochondrial permeability transition pore, decreased mitochondrial inner membrane potential (∆ψ_m), and increased caspase-like protease activity. NO-specific scavenger cPTIO enhanced these effects that were reversed by NO donor sodium nitroprusside. Our data suggest that NO suppresses Al-induced PCD by improving mitochondrial physiological properties.

Keywords: Nitric oxide; aluminum stress; mitochondria; programmed cell death.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Aluminum / toxicity*
Apoptosis / drug effects*
Caspases / metabolism*
Mitochondria / drug effects
Mitochondria / metabolism*
Nitric Oxide / metabolism*
Plants / metabolism*

Substances

Nitric Oxide
Aluminum
Caspases

Grants and funding

This work was supported by the National Natural Science Foundation of China (Nos. 31660350, 31660352, 31860334).